Raspberry Smoothie (Low-Carb) | Diabetes Strong

By electricdiet / February 16, 2021


Looking for a low-carb, vegan, on-the-go breakfast? This raspberry smoothie only takes minutes to prep and is sure to energize your morning!

Smoothie in glass with straw, topped with fresh raspberries

There’s nothing I love more than starting my day with a healthy smoothie. I look for recipes that are high in protein and low in sugar to give me sustained energy without a mid-morning crash.

This raspberry smoothie is a perfect example and one of my favorite ways to jump start my day! Two powerhouse ingredients, coconut milk and tofu, give it an irresistible creaminess along with plenty of protein and healthy fats.

Top it off with raspberries, mint leaves, a little low-carb sweetener, and some vanilla, and you have yourself a super refreshing treat. I can’t think of a better way to energize my morning.

How to make a raspberry smoothie

This delicious, healthy, satisfying smoothie comes together in less than five minutes. Just add the ingredients, blend, and serve!

Ingredients in separate ramekins, as seen from above

Step 1: Place the raspberries, mint, stevia, vanilla, and coconut milk in your blender.

Ingredients in blender, as seen from above

Step 2: Blend until completely smooth. Add the ice and blend until smooth again.

Step 3: Lastly, add the silken tofu and blend on high until completely blended.

Smoothie ingredients blended in a blender, as seen from above

Step 4: Pour, garnish with fresh raspberries and mint, if preferred, and serve.

Smoothie in a glass jar with a straw, garnished with fresh raspberries

You can sip your smoothie at home or take it on-the-go. It’s perfect no matter what you have planned for the day!

Variations for this recipe

One of my favorite parts about smoothies is how easy they are to customize. There are so many ways to get creative!

Looking to reduce the calories and fat content? Swap out some or all of the coconut milk for another low-carb plant-based milk like almond, macadamia, or hemp. If you aren’t worried about carbs, you could use oat milk as well.

Want to add even more protein? Add a scoop of pea protein powder to give yourself an extra boost.

Craving a different flavor? Use blueberries, strawberries, or mixed berries in your smoothie.

Feel free to have some fun with this yummy and versatile recipe!

Storage

This smoothie is best served fresh. I would not recommend storing it in the refrigerator.

If you only want one serving, simply halve the ingredients to blend up one smoothie. Then, you can save the rest of the ingredients for a delicious vegan smoothie to enjoy later in the week!

Raspberry smoothie in a glass jar on a wooden board, topped with fresh strawberries

Other low-carb smoothies

Looking for a few more low-carb smoothie options? There are so many yummy, diabetes-friendly options to energize your morning!

Here are a few of my favorite smoothie recipes I know you’ll love:

You can also check out my roundup of low-carb smoothie recipes for more ways to kick-start your day.

When you’ve tried this smoothie, please don’t forget to let me know how you liked it and rate the recipe in the comments below!

Recipe Card

Raspberry Smoothie (Low-Carb)

Looking for a low-carb, vegan, on-the-go breakfast? This raspberry smoothie only takes minutes to prep and is sure to energize your morning!

Prep Time:5 minutes

Total Time:5 minutes

Servings:2

Raspberry smoothie in a glass on a wooden board, topped with fresh raspberries

Instructions

  • Place the raspberries, mint, stevia, vanilla and coconut milk in your blender.

  • Blend until completely smooth. Add the ice and blend until smooth again.

  • Lastly add the silken tofu and blend on high until completely blended.

  • Pour, garnish with fresh raspberries and mint, if preferred, and serve.

Recipe Notes

This recipe is for 2 smoothies.
If you only want 1 serving, halve the ingredients. Storing this smoothie in the refrigerator is not recommend.

Nutrition Info Per Serving

Nutrition Facts

Raspberry Smoothie (Low-Carb)

Amount Per Serving (1 smoothie)

Calories 135
Calories from Fat 51

% Daily Value*

Fat 5.7g9%

Saturated Fat 2g10%

Trans Fat 0g

Polyunsaturated Fat 0.2g

Monounsaturated Fat 0g

Cholesterol 0mg0%

Sodium 21.1mg1%

Potassium 96mg3%

Carbohydrates 12.8g4%

Fiber 4.5g18%

Sugar 4.1g5%

Protein 9.8g20%

Net carbs 8.3g

* Percent Daily Values are based on a 2000 calorie diet.

Course: Breakfast, Smoothie

Cuisine: American

Keyword: dairy-free, gluten-free, smoothie, vegan, vegan smoothie



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Beef Stew in Slow Cooker Classic Easy Healthy Comfort Food

By electricdiet / February 14, 2021


Cozy Classic Comfort Food Beef Stew in Slow Cooker

Beef Stew in Slow Cooker on a cold day is hard to beat! This delicious comfort food from the Fix It Fast, Fix It Slow chapter of Guy’s Guide to Eating Well cookbook is a family favorite. Hearty and satisfying this simple to make meal practically cooks itself in the crock pot! The Beef Stew recipe calls for 10 cups total of 5 different veggies but you can use any combination of your favorite vegetables to make this delicious dish your own. Serve over couscous or rice (brown rice for extra nutrition & fiber) to soak up all of the super sauce!

Beef Stew in Slow Cooker picmonkey

Beef Stew in Slow Cooker
Simple beef stew becomes quick favorite with secret ingredient of barbecue sauce combined with meat and lots of vegetables. I like to serve over couscous or rice to soak up all the super sauce.

    Servings8 (1-cup) servings
    Prep Time15 minutes
    Cook Time5-6 hours

    Ingredients

    • 1 1/2pounds


      beef stew meat

    • 2/3cup


      sweet barbecue sauce

    • 1 1/2teaspoons


      paprika

    • 2cups


      butternut squash chunks

    • 2cups


      peeled sweet potato chunks

    • 2cups


      baby carrots

    • 2cups


      thickly sliced zucchini

    • 2cups


      thickly sliced yellow squash

    • 1/2cup


      water

    • 2cups


      baby carrots

    • 2cups


      thickly sliced zucchini

    • 2cups


      thickly sliced yellow squash

    • 1/2cup


      water

    Instructions
    1. In 3 ½-6-quart slow cooker, add all ingredients. Cook on HIGH 5-6 hours or until meat is tender.

    Recipe Notes

    Calories 231, Calories from Fat 25%, Fat 6 g, Saturated Fat 2 g, Cholesterol 53 mg, Sodium 211 mg, Carbohydrates 24 g, Dietary Fiber 3 g, Total Sugars 13 g, Protein 18 g, Diabetic Exchanges: 1 vegetable, 1 starch, ½ other carbohydrate, 2 ½ lean meat

    Terrific Tip: Use any combination of the 10 cups of vegetables

    Stock Your Kitchen for Crock Pot Cooking

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    Cookbook Full of Good For You Meals Made Simple & Delicious!

    Beef Stew in Slow Cooker is from Holly’s easy men’s cookbook – full of deliciously easy quick fix meals and crock pot cooking recipes. You won’t believe how delicious this diabetic friendly, gluten-free and freezer friendly meal is! It is easier to eat good-for-you foods in simple go-to preparation methods.

    Holly included men’s favorite recipes but made them healthier.  This book is a great resource of information as this chapter gives you the foods to fight inflammation. Plus, this cookbook entices men in the kitchen. Team Holly aims to make all meals deliciously healthy!

    Get All of Holly’s Healthy Easy Cookbooks

    The post Beef Stew in Slow Cooker Classic Easy Healthy Comfort Food appeared first on The Healthy Cooking Blog.



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    Managing Hyperglycemia in the COVID-19 Inflammatory Storm

    By electricdiet / February 12, 2021


    A new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease 2019 [COVID-19]) was first reported in late December 2019 in Wuhan, China (1), and has progressed to become a pandemic with over 3 million cases confirmed (2) and still growing (3). No specific therapeutic agents have been identified, and its infectious nature, hospitalization rates, intensive care admissions, and mortality are very high (2,47). Preexisting chronic illnesses such as diabetes, hypertension, and obesity result in worst outcomes in the presence of COVID-19 infection and virus-induced respiratory dysfunction (8). In influenza-like illnesses, hyperglycemia has been reported to increase plasma glucose concentration in airway secretions. Additionally, increased viral replication in vivo and suppression of the antiviral immune response is also described (9). Increased permeability of the vasculature and subsequent collapse of alveolar epithelium have direct effects on pulmonary function (10) and may explain the higher mortality rates observed in these patients (8).

    Hyperglycemia and COVID-19 Infections

    The significant hyperglycemia that occurs in the acute inflammatory state of COVID-19 patients has been recognized and found to be pronounced among those with diabetes, prediabetes, and/or obesity. A bidirectional link between chronic inflammation and hyperglycemia had been already described for chronic complications of diabetes. For instance, several changes in the immune system including alterations in specific cytokines and chemokines, shifts in the number and activation state of various leukocyte populations, and increased apoptosis and tissue fibrosis are present in obesity and type 2 diabetes, suggesting that inflammation has an active role in the pathogenesis of hyperglycemia, progression to clinically overt type 2 diabetes, and chronic complications (1114). We believe that this baseline inflammatory state could set the stage and background for further elevations in the levels of inflammatory cytokines, particularly as seen in acute infectious diseases such as COVID-19, further increasing insulin resistance, promoting proinflammatory effects of acute (stress) hyperglycemia, and ultimately leading to a poor prognosis of such patients with diabetes (1518). Our observations are corroborated by the recent retrospective multicentered study of over 7,000 cases of COVID-19 in Hubei Province, China (17). The authors reported a significant correlation between well-controlled blood glucose and lower serum levels of inflammatory markers (interleukin-6 [IL-6], high sensitivity C-reactive protein [hsCRP], lactate dehyrogenase [LDH]) in patients with COVID-19. A recently reported study in patients with diabetes without advanced chronic complications or comorbidities at baseline supports the marked and rapidly evolving inflammatory process in the presence of SARS-CoV-2 infection (19). Despite presenting initially with mild symptoms and fever, the clinical course deteriorated very rapidly with progressive dyspnea and pneumonia with higher computerized tomography imaging severity scores. Compared with patients without diabetes, individuals with diabetes showed higher elevations in the concentrations of IL-6, ferritin, hsCRP, and d-dimer foreshadowing a raging cytokine storm and a hypercoagulable state with rapid deterioration. In addition, the insulin requirements were very high even in those patients who were insulin naive prior to admission (19).

    Although the current information continues to emerge and the full impact of severely high peaks in glucose levels on disease course and mortality has only recently become available, the initial experience we collected since the peak of COVID-19 in Michigan suggests that acute and persistent surges in blood glucose levels associated with the cytokine storm herald poor prognosis. Thus, in conjunction with management of infection, inflammation, and supportive care, a rapidly instituted and tailored glucose management plan targeting hyperglycemia is critical. This can help prevent and reduce morbidity and complications leading to prolonged inpatient stay and increased resource utilization during these times when most hospitals and health care systems are overwhelmed by the COVID-19 cases (17).

    Michigan is one of the states with a very high number of COVID-19 cases and high rates of complications and mortality. Here we provide a perspective on the Michigan Medicine experience and the plans implemented to effectively curb these glucose surges and expedite recovery for patients with diabetes and/or stress hyperglycemia admitted with COVID-19–related illness.

    Intervention

    A specialized regional isolation containment unit was created for the acute care of these patients, and a stepwise general management plan that also included specified laboratory testing to monitor disease activity with a panel of inflammatory and prothrombotic markers was implemented. The overall health care delivery models have been transformed significantly, transitioning from the classical in-person consult to interprofessional consultations. This model relies on interactive chart reviews and provides recommendations to the primary teams by diabetes specialists with the goal of preserving personal protective equipment (PPE) and reducing exposure for health care providers.

    Within the very first days of COVID-19 inpatient surge, a phenotype of severe hyperglycemia was noted in a large proportion of the critically ill admitted patients carrying a prior diagnosis of type 1 diabetes, type 2 diabetes, prediabetes, or severe obesity. Their glucose management was further complicated by rapid acute renal failure, tube feed initiation, vasopressor support for hypotension, steroids for acute respiratory distress syndrome, and chronic renal replacement therapy. In addition, detailed history of their diabetes management was limited, as several patients were transferred from other Michigan hospitals not connected with our electronic medical records. All these factors presented important health care challenges.

    Thus, our major aim was to develop viable algorithms to provide a targeted approach to manage hyperglycemia in COVID-19–infected patients based on a personalized risk stratification that includes different levels of hyperglycemia and insulin resistance, prior diabetes control, presence of obesity, needs and type of nutritional support, renal dysfunction, vasopressor support, and disease activity.

    The University of Michigan Hospital provided care to ∼500 COVID-19 patients since the COVID-19 crisis hit southeast Michigan. Approximately 160 out of 500 patients had known diabetes and were referred to us for management. However, some patients who came in critical condition and had no prior known diabetes also developed hyperglycemia. We also observed that among patients we followed, ∼43% were African American, which is high but in line with other observations showing a disproportionately high burden of severe disease among African Americans (20). The algorithm was rapidly developed, and although it continued to be refined daily in the first couple of weeks based on the emerging observations by our team, it is fair to state that it was used in a more or less refined form in up to 200 patients. In addition, given the very large number of patients we had to follow on a daily basis, we have activated several hyperglycemia management teams to cover all these patients.

    Preliminary in-house experience has confirmed that the severity of hyperglycemia and marked insulin resistance were also associated with a characteristic inflammatory biomarker signature that includes rapid elevations and changes in the levels of hsCRP, procalcitonin, triglycerides, IL-6, and d-dimers; thus, these were also included in the risk stratified approach. Several prior studies have reported that procalcitonin levels may be important predictors for a more severe form of disease (17,21). See examples in two randomly selected patients admitted with COVID-19–related pneumonia, acute respiratory distress syndrome, and important surges in inflammatory biomarkers who developed severe hyperglycemia followed by our team (Fig. 1A and B).

    Figure 1
    Figure 1

    Examples of randomly selected patients admitted with COVID-19–related pneumonia, acute respiratory distress syndrome, and important surges in inflammatory biomarkers who developed severe hyperglycemia in the presence of cytokine storm. Data are shown for procalcitonin, blood glucose levels, and insulin requirement during the acute inflammatory surge in two randomly selected patients: patient A, well controlled prior to admission on oral antiglycemic agents, and patient B, requiring prior insulin.

    In the next steps, we created protocols for insulin delivery for nurses entering individual patient rooms. We prioritized reducing the number of glucose checks as much as safely possible in order to minimize health care providers’ exposures while also conserving PPE. The U.S. Food and Drug Administration recently approved the use of continuous glucose monitors for inpatient glucose measurements (22). While this definitely helps in reducing exposure and conserving PPE, in our experience, their accuracy is not validated in the most critical patients due to superimposed hypotension, use of vasopressors, and possibly high-dose acetaminophen, which can falsely elevate glucose levels. Additionally, given the complex care of these patients, the extra burden of teaching the use of a new tool on nurses was not sustainable. Thus, for convenience, we included arterial and venous blood glucose values, which are frequently drawn in ventilated patients and in patients receiving high dose of intravenous vitamin C infusion, to replace point-of-care glucose checks, and we reduced the number of glucose checks to every 6 h in the majority of cases. To further reduce burden on primary teams, and for timely insulin dose adjustments to parallel changes in inflammatory and the rest of disease progress markers, our team was performing insulin dose adjustments multiple times a day and was in charge of writing all insulin orders for inpatient hyperglycemia management. This was a critical component for success, given the very fluid clinical status of the severely ill COVID-19 patients, necessitating a very close watch and constant changes in insulin regimens for successful titrations.

    The tailored protocols developed are described in Tables 1 and 2 with overall targeted blood glucose goals of 150–180 mg/dL. However, blood glucose levels <200 mg/dL were also targeted in some patients with very labile and critical forms of disease, particularly since most were also on continuous tube feeding and thus in a constant postprandial state.

    Table 1

    Initial subcutaneous insulin dosing guideline for critically ill COVID-19 patients admitted with high glucose

    For critically ill patients with severe hyperglycemia (blood glucose >450 or 500 mg/dL), an insulin infusion was initiated with titration often requiring very high rates—up to 12–20 units/h and occasionally up to 40 units/h. Once glucose ranges were within 200–300 mg/dL at lower hourly insulin drip rates, we would transition to subcutaneous insulin as soon as possible given the extenuating health care considerations described above.

    Scheduled regular insulin, a sliding scale, and basal insulin adequately timed with other nursing interventions, especially arterial blood gas checks for ventilator settings, helped successfully lower glucose levels into goal range without increasing nurse contact, thus decreasing overall burden and PPE use. Our algorithms to predict labile glucose values with significant hyper- and hypoglycemia were improved by monitoring the changes in inflammatory biomarkers levels checked by the intensive care unit (ICU) teams, thus allowing us to prompt up or down titrations of insulin doses more confidently to prevent either further glucose surges or hypoglycemia. Given that insulin resistance reduces dramatically as a patient’s clinical condition improves, we proactively reduced insulin doses as soon as reductions in inflammatory biomarkers trends were documented. This flexible approach following trends in frequently monitored inflammatory markers to help us guide insulin titrations was a critical part of our evaluation. Our observations and developed algorithms were in fact in concordance with the recent publication by Hamdy and Gabbay (23) outlining a similar experience and administration of regular insulin every 6 h in the management of diabetes in COVID-19 patients in ICU at the Joslin Diabetes Center. In addition, similar to our Perspective, the recent review by Al-Jaghbeer and Lansang (24) provides broad guidance in management of hyperglycemia in COVID-19 patients in ICU.

    Our Perspective has several limitations. First, the data described and the algorithm we have developed are not a result of a randomized clinical trial or a research study but instead are based on our direct observations in the patients with severe COVID-19 disease we followed. Thus, we do not have a control population to compare differences in outcomes. Second, we acknowledge that given the very fluid status associated with this pandemic and the rapid rise in the number of severe cases admitted, there are many confounding factors that we are unable to account for at this time. In addition, we are unable to provide at this time more specific data on the direct effectiveness of this algorithm on several important outcomes such as mortality, time to recovery, length of intensive care or overall hospital stay, or rate of severe complications associated with the algorithm. Lastly, these initial observations may only be applicable to patients with phenotypes and socioeconomic status similar to those who were admitted to the University of Michigan Hospitals. Thus, these need to be confirmed in larger and controlled studies that are including the new evidences on disease course, risk factors, management, and prognosis of COVID-19 infection that are emerging globally.

    Strengths of the algorithm are the fact that the continuous management of the insulin orders by our diabetes team allowed us to proactively and effectively react to surges in glucose levels driven by disease activity and significantly decrease the burden on the primary teams.



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    Grilled Turkey Tenderloin with Berry Chipotle Sauce

    By electricdiet / February 10, 2021


    This grilled turkey tenderloin with berry chipotle sauce is smoky and a little sweet, with just a bit of heat from the chiles and a burst of tang from the balsamic!

    Grilled Turkey Tenderloin with Berry Chipotle Sauce cut into slices and served over greens on a platter

    Turkey is a very lean and healthy protein. But since it has a pretty mild flavor, I always like adding some kind of flavorful sauce to compliment the dish.

    This grilled turkey tenderloin with berry chipotle sauce is absolutely bursting with flavor! And you only need 5 ingredients plus salt, pepper, and oil to make it.

    It’s a great way to liven up your cooking routine. The smokiness from the grill, sweetness from the berries, little kick of heat from the chiles, and burst of tang from the balsamic come together into one delicious dish!

    So when you’re looking for an amazing meal that you can feel good about eating, give this grilled turkey with berry chipotle sauce a try.

    How to make grilled turkey tenderloin with berry chipotle sauce

    This recipe involves making the sauce in one pot on the stove, then throwing the turkey on the grill. It’s so easy to prep!

    Step 1: In a small saucepan, combine the fruit, honey, vinegar, chipotle, and adobo sauce. If the mixture seems dry, add 1 tablespoon water.

    Step 2: Bring to a boil, then reduce the heat and simmer, stirring occasionally.

    Step 3: As the mixture simmers, smash the berries against the side of the pan with a wooden spoon. Continue cooking until the berries have mostly disintegrated, about 10 minutes.

    Step 4: Pour the mixture through a strainer into a bowl. To extract as much liquid as possible, press the mixture firmly against the strainer and scrape the bottom of the strainer occasionally with a separate spoon. Discard the solids.

    Step 5: Preheat the grill.

    Step 6: Rub each tenderloin with about 1 tablespoon of olive oil, then season with salt and pepper.

    Step 7: Transfer to the grill and cook, turning a few times, until the turkey reaches an internal temperature of 165°F, about 20-25 minutes.

    Turkey on the grill with a cooking thermometer
    The turkey still need a few minutes to reach a core temperature of 165 F

    Step 8: Place the turkey on a cutting board and let it rest for about 10 minutes.

    Step 9: Cut the turkey into thin slices and serve with the sauce.

    Once you try this delicious dish, you may start adding it to your menu all the time!

    Variations for the sauce

    The turkey tenderloin is quite tasty on its own, but if we’re being honest, the berry chipotle sauce is really what makes this dish so special. So if you want to customize it to your tastes, please feel free!

    I used frozen berries for convenience, but you could also use fresh berries if they’re in season. Any combination of raspberries, strawberries, blueberries, and blackberries works well!

    Want a bright-red sauce that really makes a statement? Make the sauce with just raspberries to get that vibrant pop of color.

    If you aren’t a big fan of spicy food, start with just a little bit of the adobo sauce. If the sauce turns out too spicy, add in more fruit or honey. The sweetness will help balance out the heat.

    Storage

    If you have any leftovers, try to store the turkey and the sauce separately if possible. This will help them stay fresh the longest.

    Simply place them in separate airtight containers in the refrigerator. The turkey should be enjoyed within 3-4 days, and the sauce will stay fresh for up to a week.

    Slices of turkey tenderloin with sauce on top

    Other delicious turkey recipes

    Looking for more fun and exciting dishes you can make with lean and healthy turkey? Here are a few of my favorite recipes I know you’ll love:

    When you’ve tried this dish, please don’t forget to let me know how you liked it and rate the recipe in the comments below!

    Recipe Card

    Grilled Turkey Tenderloin with Berry Chipotle Sauce cut into slices and served over greens on a platter

    Grilled Turkey Tenderloin with Berry Chipotle Sauce

    This grilled turkey tenderloin with berry chipotle sauce is smoky and a little sweet, with just a bit of heat from the chiles and a burst of tang from the balsamic!

    Prep Time:5 minutes

    Cook Time:35 minutes

    Rest Time:10 minutes

    Total Time:50 minutes

    Author:Diabetic Foodie

    Servings:4

    Instructions

    • In a small saucepan, combine the fruit, honey, vinegar, chipotle, and adobo sauce. If the mixture seems dry, add 1 tablespoon water.

    • Bring to a boil, then reduce the heat and simmer, stirring occasionally.

    • As the mixture simmers, smash the berries against the side of the pan with a wooden spoon. Continue cooking until the berries have mostly disintegrated, about 10 minutes.

    • Pour the mixture through a strainer into a bowl. To extract as much liquid as possible, press the mixture firmly against the strainer and scrape the bottom of the strainer occasionally with a separate spoon. Discard the solids.

    • Preheat the grill.

    • Rub each tenderloin with about 1 tablespoon of olive oil, then season with salt and pepper.

    • Transfer to the grill and cook, turning a few times, until the turkey reaches an internal temperature of 165°F, about 20-25 minutes.

    • Place the turkey on a cutting board and let it rest for about 10 minutes.

    • Cut the turkey into thin slices and serve with the sauce.

    Recipe Notes

    This recipe is for 4 servings of turkey tenderloin and berry chipotle sauce.
    If you use fresh berries instead of frozen, add about 1 tablespoon of water since you won’t have any extra liquid from thawing.
    For a bright red sauce, only use raspberries.
    If your sauce turns out too spicy for you, add in more fruit or honey. The sweetness will balance out the heat.
    If you have leftovers, store the turkey and the sauce in separate airtight containers in the refrigerator. The turkey should be enjoyed within 3-4 days, and the sauce will stay fresh for up to a week.

    Nutrition Info Per Serving

    Nutrition Facts

    Grilled Turkey Tenderloin with Berry Chipotle Sauce

    Amount Per Serving

    Calories 359
    Calories from Fat 137

    % Daily Value*

    Fat 15.2g23%

    Saturated Fat 3.2g20%

    Trans Fat 0g

    Polyunsaturated Fat 3.5g

    Monounsaturated Fat 2.5g

    Cholesterol 104mg35%

    Sodium 584mg25%

    Potassium 3mg0%

    Carbohydrates 12.9g4%

    Fiber 0.9g4%

    Sugar 9.3g10%

    Protein 42.2g84%

    Net carbs 12g

    * Percent Daily Values are based on a 2000 calorie diet.

    Course: Main Course

    Cuisine: American

    Diet: Diabetic, Gluten Free

    Keyword: easy dinner recipes, grilled turkey tenderloin



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    Pretzel Pizza – My Bizzy Kitchen

    By electricdiet / February 8, 2021





    Pretzel Pizza – My Bizzy Kitchen




































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    What is Brittle Diabetes: Diagnosis and Treatment

    By electricdiet / February 6, 2021


    Also referred to as “hard to control” diabetes or “labile” diabetes, brittle diabetes is a term to describe type 1 diabetes that is very difficult to manage.

    The term “brittle diabetes” has been long debated in the endocrinology world because anyone with type 1 diabetes knows that just one unit of too much or too little insulin can easily lead to quick swings in your blood sugar.

    This can be a controversial issue, as some people believe it’s an outdated label for a condition that’s so hard to manage, some insist that it simply doesn’t exist, and others feel that being diagnosed as “brittle” is accusatory, or an insult that you’re not staying on top of your diabetes. 

    However, the category stands, and people with diabetes are regularly diagnosed as being “brittle”. So, what exactly is brittle diabetes? 

    In this article, we’ll discuss what brittle diabetes is, the risk factors, how it’s diagnosed, and the best ways to manage it for smoother blood sugar levels.

    What is “brittle” diabetes?

    Those with brittle diabetes can see blood sugars swing wildly high and low without explanation or logical predictability, often resulting in frequent hospitalization. These swings negatively disrupt their overall quality of life. 

    Those with brittle diabetes also typically struggle with hypoglycemia unawareness, which means they’ve experienced so many severe low blood sugars, their body no longer alerts them to oncoming lows with traditional symptoms, such as shakiness, sweating, confusion, and rapid heart rate. 

    According to the National Institutes of Health, only a small percentage of people with type 1 diabetes experience these drastic fluctuations in blood sugars that can frequently be described as “brittle”, affecting only 3 out of every 1,000 people with type 1 diabetes. Younger, heavyset women between the ages of 15-30 are most likely to be affected by brittle diabetes. 

    Risk factors for brittle diabetes

    The most significant risk factor for brittle diabetes is type 1 diabetes, as brittle diabetes is a subset of the disease. Other risk factors include anxiety, depression, and high levels of stress

    People who frequently find themselves in high-stress situations release more of the hormone cortisol, which increases insulin resistance, spiking blood sugars, and worsening blood sugar fluctuations. 

    Some people with type 1 diabetes may produce abnormal and inconsistent amounts of glucagon, a hormone that tells your liver to produce glucose. This can easily lead to rapid swings in blood sugar levels, resulting in a diagnosis of brittle diabetes. 

    Additionally, those suffering from gastroparesis or celiac disease may experience brittle diabetes, due to malabsorption of nutrients and carbohydrates, which can result in unpredictable insulin requirements. 

    If your meals are being digested inconsistently, it can create sudden spikes or drops in blood sugar because the timing of your insulin dose is impossible to match with the unpredictable digestion of your meal. 

    Young women who have a history of eating disorders, such as diabulimia, anorexia nervosa, bulimia, or binge eating disorder are also at a higher risk for brittle diabetes. 

    Diagnosis

    Getting the correct diagnosis for brittle diabetes can prove difficult. Many times, brittle diabetes is diagnosed concurrently with mental health issues, such as depression. 

    For example, a person suffering from depression may forget to pre-bolus for a meal (or bolus at all), which can exacerbate fluctuations in blood sugars, and out of control blood sugar levels can worsen depression and anxiety; oftentimes these conditions feed into each other. 

    One study showed that people with brittle diabetes have a greater hormonal response to stress, and release more cortisol (causing more insulin resistance) than those without brittle diabetes.

    Treatment options

    The treatment of brittle diabetes will often include treating any underlying psychological or mental health issues first, controlling the level of stress (and subsequent hormonal response) one is experiencing.

    Behavioral therapy is typically effective in treating those with brittle diabetes and achieving better health outcomes, including improved blood sugar levels and Hba1c results.

    Those with brittle diabetes may require a long hospitalization where food intake, insulin dosage exercise routines, and the stress response is monitored closely, to achieve baseline data for more successful long-term treatment protocol and control. 

    Some other helpful ways to treat brittle diabetes include:

    • Wearing a continuous glucose monitor to track blood sugar trends
    • Re-establishing sensitivity to low blood sugars, by working closely with your doctor 
    • Using an insulin pump for more precise dosing 
    • Reducing carbohydrates, and having a more predictable diet 
    • Having a regular, consistent exercise routine
    • Getting the proper amount of sleep each night
    • Managing stress in healthy ways, such as practicing yoga and meditation 

    Living well with brittle diabetes 

    Getting an official diagnosis of brittle diabetes is rare and usually accompanies underlying mental health or gastrointestinal disorders.

    It’s normal for people with type 1 diabetes to have extreme fluctuations in blood sugar, and for it not to be officially characterized as brittle diabetes. 

    Life with diabetes is complicated, and the learning curve is neverending. Long-term success in living with diabetes comes down to a constant effort to study and learn about your blood sugar levels and insulin needs around life’s many variables.

    However, if you feel that you may have this rare condition, call your doctor right away. The first step in addressing brittle diabetes comes down to working with an expert Certified Diabetes Educator or diabetes coach and improving how you take your insulin, how you eat, how and when you exercise, and how you manage the variables that impact blood sugar levels the most.

    Hospitalizations are much more common in people with brittle diabetes, making school and work attendance more difficult. People with brittle diabetes are also much more vulnerable to experiencing a diabetic coma from lows and diabetic ketoacidosis (DKA) from highs. 

    Talking with your doctor can help you get the right diagnosis for this condition, and they can help you make a plan to better manage it, and address any underlying mental health or digestive issues that may be contributing to such wild swings in blood sugar levels. 

    Type 1 diabetes is always challenging, but with enough gradual education, you can likely gain more confidence and understanding of how to improve your blood sugar levels, your safety, and your quality of life.



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    Greek Chicken Burgers – Healthy Easy Diabetic Friendly Meal

    By electricdiet / February 4, 2021


    Fantastic Diabetic Friendly High Protein Greek Chicken Burgers

    Shake up your usual burger routine with these delicious Greek Chicken Burgers from Holly Clegg’s Guy’s Guide to Eating Well cookbook. Fantastic flavor with a few healthy Mediterranean style ingredients makes this hearty satisfying burger not only fantastic tasting but good for you too! This is also a great source of lean protein which helps build and repair muscle. Make them ahead of time and freeze uncooked burgers to pull out on busy nights. For sliders, make 12 miniature patties.

    Greek Chicken Burgers picmonkey 2

    Greek Chicken Burgers
    Get out of your comfort zone and try this amazing chicken burger with Greek flair. Serve with sliced red onion, tomato and cucumber.

      Servings4 burgers
      Prep Time10 minutes
      Cook Time15 minutes

      Ingredients

      • 1pound


        ground chicken

      • 1


        large egg white

      • 1/3cup


        dried bread crumbs

      • 1teaspoon


        minced garlic

      • 2teaspoons


        dried oregano leaves

      • 1/2cup


        coarsely chopped baby spinach leaves

      • 1/4cup


        crumbled reduced-fat feta cheese



      • salt and pepper to taste

      • 2teaspoons


        dried oregano leaves

      • 1/2cup


        coarsely chopped baby spinach leaves

      • 1/4cup


        crumbled reduced-fat feta cheese



      • salt and pepper to taste

      Instructions
      1. Preheat oven 500°F. Line baking sheet with foil.

      2. In large bowl, combine all ingredients and form into four patties. Cook 15 minutes or until done.

      Recipe Notes

      Calories 192 kcal, Calories from Fat 22%, Fat 5 g, Saturated Fat 2 g, Cholesterol 75 mg, Sodium 333 mg, Carbohydrates 8 g, Dietary Fiber 1 g, Total Sugars 1 g, Protein 28 g, Dietary Exchanges: 1/2 starch, 3 lean meat

      Terrific Tip: Make ahead and freeze uncooked burgers to pull out on busy nights. For sliders, make 12 miniature patties.

      Greek Chicken Burgers

      Cookbook Full of Good For You Meals Made Simple & Delicious!

      Greek Chicken Burgers is a diabetic friendly recipe from the GERD chapter in Holly’s easy men’s cookbook. Weight loss is often a successful step in reducing GERD because belly fat worsens reflux symptoms. Hand in hand with obesity, diabetes can also be an underlying cause of GERD. By choosing trim and terrific, high fiber, unprocessed whole foods, lean meat, fruits and vegetables, you will start reducing your weight and in turn reducing your risk for GERD.

      Holly included men’s favorite recipes but made them healthier.  This book is a great resource of information as this chapter gives you the foods to fight inflammation. Plus, this cookbook entices men in the kitchen. Team Holly aims to make all meals deliciously healthy!

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      The post Greek Chicken Burgers – Healthy Easy Diabetic Friendly Meal appeared first on The Healthy Cooking Blog.



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      The Role of Glucagon in the Acute Therapeutic Effects of SGLT2 Inhibition

      By electricdiet / February 2, 2021


      Abstract

      Sodium–glucose cotransporter 2 inhibitors (SGLT2i) effectively lower plasma glucose (PG) concentration in patients with type 2 diabetes, but studies have suggested that circulating glucagon concentrations and endogenous glucose production (EGP) are increased by SGLT2i, possibly compromising their glucose-lowering ability. To tease out whether and how glucagon may influence the glucose-lowering effect of SGLT2 inhibition, we subjected 12 patients with type 2 diabetes to a randomized, placebo-controlled, double-blinded, crossover, double-dummy study comprising, on 4 separate days, a liquid mixed-meal test preceded by single-dose administration of either 1) placebo, 2) the SGLT2i empagliflozin (25 mg), 3) the glucagon receptor antagonist LY2409021 (300 mg), or 4) the combination empagliflozin + LY2409021. Empagliflozin and LY2409021 individually lowered fasting PG compared with placebo, and the combination further decreased fasting PG. Previous findings of increased glucagon concentrations and EGP during acute administration of SGLT2i were not replicated in this study. Empagliflozin reduced postprandial PG through increased urinary glucose excretion. LY2409021 reduced EGP significantly but gave rise to a paradoxical increase in postprandial PG excursion, which was annulled by empagliflozin during their combination (empagliflozin + LY2409021). In conclusion, our findings do not support that an SGLT2i-induced glucagonotropic effect is of importance for the glucose-lowering property of SGLT2 inhibition.

      Introduction

      Sodium–glucose cotransporter 2 inhibitors (SGLT2i) are glucose-lowering agents that lower plasma glucose (PG) concentrations by increasing urinary glucose excretion (1,2). SGLT2 is highly expressed in the proximal renal tubule and accounts for the majority of reabsorption of glucose filtered through the glomeruli (3). In type 2 diabetes, SGLT2i improve glycemic control, with a low rate of hypoglycemia and body weight loss as an additional advantage (46). Another attractive feature of SGLT2i is a reduced risk of major adverse cardiovascular events in high-risk patients (7,8). SGLT2i have been reported to increase glucagon concentrations and augment endogenous glucose production (EGP) in mice (9) as well as in individuals with type 2 diabetes (1012). The reported glucagonotropic effect of SGLT2i may reflect a compensatory mechanism caused by declining blood glucose or glucosuria and/or could be a direct effect of the SGLT2i on the pancreatic α-cells (9). In support of the latter, expression of SGLT2 in the pancreatic α-cells has been described (9,13,14). However, conflicting data are emerging, and the direct effect of SGLT2i on 1α-cells is under debate (15,16).

      Patients with type 2 diabetes are characterized by fasting hyperglucagonemia, and inappropriate suppression of glucagon together with increased EGP after meal intake (17,18) have previously been linked to postprandial hyperglycemia in type 2 diabetes (19,20). Thus, further augmentation of glucagon levels during SGLT2i treatment may attenuate the glucose-lowering effect of this drug class. Therefore, the concept of combining SGLT2i with agents counteracting glucagon-mediated effects on EGP has received much attention (18,21). Clinical studies investigating combination therapy with glucagon-like peptide 1 (GLP-1) receptor agonist (lower glucagon levels and reduced EGP) and SGLT2i in patients with inadequately controlled type 2 diabetes have shown additive glucose-lowering effects (22,23). Antagonization of the glucagon receptor represents another strategy to reduce hyperglucagonemia-associated hyperglycemia in type 2 diabetes (18,2426). However, the clinical development of several glucagon receptor antagonists (GRAs) has been discontinued because of side effects, including hepatic steatosis and increased concentrations of total cholesterol, LDL cholesterol, and hepatic transaminases (2628), combined with concerns about α-cell hyperplasia in preclinical studies (26). Here, we tested the hypothesis that a glucagonotropic effect of SGLT2i would affect the glucose-lowering effect of SGLT2i in type 2 diabetes by applying single doses of the SGLT2i empagliflozin with and without the GRA LY2409021 in a randomized, placebo-controlled, double-blinded, crossover study involving four liquid mixed-meal tests (MMTs) in patients with type 2 diabetes.

      Research Design and Methods

      Ethical Approval

      This study protocol was approved by the ethical committee of The Capital Region of Denmark (H-15018701), and the study was conducted in accordance with standards of good clinical practice, the Declaration of Helsinki, and all applicable local regulations.

      Participants

      Patients with type 2 diabetes were recruited from the diabetes outpatient clinic at the Department of Medicine, Gentofte Hospital, or by advertising. Thirteen patients were included (12 completed) on the basis of the following inclusion criteria: Caucasians >30 years of age with diet- and/or metformin-treated type 2 diabetes diagnosed according to the World Health Organization (29) for at least 3 months and a normal hemoglobin. The following exclusion criteria were used: inflammatory bowel disease, intestinal resections, nephropathy (serum creatinine above normal range and/or albuminuria), known or suspected liver disease (hepatic transaminases elevated more than two times the upper normal level), treatment with medicine that could not be paused for 12 h, loop diuretics or glucose-lowering medications other than metformin, pregnancy and/or breastfeeding, family history of pancreatic islet tumors, age >70 years, and chronic heart failure.

      Study Medication

      GRA LY2409021 was provided as a gift from Eli Lilly (Indianapolis, IN). In clinical trials, this selective, orally administered, competitive, small-molecule GRA has a median time for maximum drug concentration (Tmax) ranging from 4 to 8 h and a mean half-life (T1/2) ranging from 51 to 59 h (30). A dose of 300 mg at the start of the fast the evening before the experimental day was chosen to achieve near-maximal glucagon receptor antagonism and clear reduction of EGP during the following study day (30,31). The SGLT2i empagliflozin has a Tmax of 1–2 h and a T1/2 of ∼12 h after single-dose administration of 25 mg, and it was therefore administered 2 h before meal ingestion (with 50 mL water) and expected to result in near-maximum inhibition during the mixed meal (1,32).

      Study Design and Experimental Procedures

      This study was a double-blinded, placebo-controlled, double-dummy, crossover study consisting of a screening visit and 4 experimental days performed in randomized order: 1) placebo + placebo, 2) SGLT2i (empagliflozin 25 mg) + placebo, 3) GRA (LY2409021 300 mg) + placebo, and 4) GRA (LY2409021 300 mg) + SGLT2i (empagliflozin 25 mg). Days were separated by a minimum of 2 weeks to ensure washout of LY2409021. All experiments were performed at Gentofte Hospital, University of Copenhagen. Glucose-lowering treatment was paused for 1 week before each study day. Participants met in the morning after a 10-h fast (including liquids, medicine, and tobacco), and were placed in a hospital bed in a semirecumbent position. Two cannulas were inserted in the cubital veins: one for infusions and one in the contralateral arm for collection of arterialized blood samples using the heated hand technique (hand and forearm wrapped in heating pad at ∼45°C). At time −120 min, empagliflozin/placebo was ingested (with 50 mL water), and a primed constant infusion of stable isotopes (Cambridge Isotope Laboratories, Tewksbury, MA) dissolved in saline was initiated ([6,6-2H2]glucose [priming dose 17.6 μmol × kg−1 fasting PG (FPG) / 5 and constant infusion of 0.6 μmol × kg−1 × min−1] and [1,1,2,3,3-D5]glycerol [priming dose 2 μmol × kg−1 and constant infusion of 0.1 μmol × kg−1 × min−1]). At time 0 min, participants ingested a standardized liquid MMT (47.2 g anhydrous glucose, 15.2 g whey protein powder, and 14.1 g grapeseed oil mixed in 150 mL water; 200 mL, 394 kcal, 50 proportion of energy (%E) carbohydrates, 15%E protein, and 35%E fat) over a period of 10 min. Acetaminophen (1.5 g) was added to the liquid meal for evaluation of gastric emptying rate (33,34) and 2.8 g [U-13C6]glucose for tracing the orally ingested glucose (double-tracer technique) (35,36). After the 4-h MMT, participants were served an ad libitum meal of pasta Bolognese (energy content per 100 g: 147 kcal, 17.4 g carbohydrates, 5.6 g protein, 5.9 g fat) and were told to eat until pleasantly satiated.

      Data Collection

      Before initiation of experimental procedures, participants were instructed to empty their urinary bladder and again at time 240 min; urine volume was registered, and samples were collected and stored at −20°C for subsequent measurements of glucose and tracer concentrations. Blood samples were drawn at time −120, −45, −30, −15, 0, 10, 20, 30, 50, 70, 90, 120, 150, and 240 min. For bedside measurements of PG, blood was collected in sodium fluoride–coated tubes and centrifuged immediately (30 s, room temperature, 7,500g). Blood for the analysis of glucagon and isotope enrichments was collected in prechilled EDTA tubes with dipeptidyl peptidase 4 inhibitor (valine pyrrolidide 0.01 mmol/L; gift from Novo Nordisk, Måløv, Denmark). Samples collected in lithium heparin tubes (acetaminophen) and dry tubes with serum separator gel and silica particles for clot activation (C-peptide) were left to coagulate (20 min, room temperature). All blood samples were centrifuged (15 min, 4°C, 2,900g) and stored afterward at −20°C (plasma) or −80°C (serum) until study completion and later analysis. Energy intake during the ad libitum meal was calculated by subtracting the amount of weighed leftovers from the amount of weighed food served. Resting energy expenditure and respiratory quotient were measured by indirect calorimetry with a tight face mask, measuring gas exchange breath by breath (CCM Express; MedGraphics Diagnostics, St. Paul, MN), for 12 min at baseline before the MMT and at time 30 min.

      Laboratory Methods

      PG was analyzed at bedside using the glucose oxidase method (Model 2300 Stat Plus and 2900 Biochemistry Analyzers; Yellow Springs Instruments, Yellow Springs, OH). Glucose and glycerol concentrations and plasma enrichments of [6,6-2H2]glucose, [1,1,2,3,3-D5]glycerol, and [U-13C6]glucose were measured by liquid chromatography-tandem mass spectrometry as previously described (37). Serum C-peptide was measured using a two-site sandwich immunoassay with direct chemiluminescent technology (ADVIA Centaur XP; Siemens Healthcare A/S, Ballerup, Denmark). Plasma acetaminophen analysis was based on amidase hydrolysis, oxidation, and linkage to tetrahydroquinoline, producing a color shift measured by reflectance photometry (670 nm) (Vitros 5.1 FS; Ortho-Clinical Diagnostics). Plasma glucagon was measured with an in-house radioimmunoassay (antibody 4305) directed against the COOH-terminal (38), which has been validated thoroughly as recently discussed (39).

      Calculations and Statistical Analyzes

      Results are reported as mean ± SEM unless otherwise stated. Area under the curve (AUC) was calculated using the trapezoidal rule. Statistical comparisons were made with a linear mixed model, with experimental day as the fixed effect and with an unstructured covariance pattern to account for correlation between repeated measurements in the same individual. Mixed-model analyses were performed with SAS Enterprise Guide 7.1 (SAS Institute, Cary, NC) (40). To reduce the risk of false positives as a result of multiple testing, all P values were adjusted (adj.) using the method of Benjamini and Hochberg (41) to control the false discovery rate (i.e., an adj. P ≤ 0.05 means that the reported significance is ≤5% likely to be false positive). All participants included in the analyses completed all experimental days. Tracer isotope data are displayed as glucose Ra and Rd calculated from changes in glucose enrichment using Steele’s one-compartment, fixed-volume (fixed pool fraction of 70 mL × kg−1), nonsteady-state model for stable isotopes (42). Insulin secretion rate (ISR) was calculated by deconvolution of C-peptide and C-peptide kinetics (43,44). HOMA insulin resistance was calculated from fasting C-peptide and glucose with HOMA calculator version 2.2.3 software (Diabetes Trials Unit, University of Oxford, https://www.dtu.ox.ac.uk/homacalculator).

      Data and Resource Availability

      The data sets generated and analyzed during the current study are not publicly available but are available from the corresponding author upon reasonable request.

      Results

      Participant Characteristics

      In total, 13 patients were randomized. Twelve patients with type 2 diabetes completed all 4 study days and were included in the study (Table 1). Eleven patients were treated with metformin only (well controlled on 0.5–2 g daily), and one patient was treated with diet only. One participant with a history of migraines dropped out after the 2nd experimental day (not included in analyses) because of a migraine after the 1st experimental day. This participant was replaced by another to ensure 12 completing participants.

      Table 1

      Participant characteristics

      Glucose Concentrations

      FPG was lowered by both empagliflozin and LY2409021 compared with placebo (mean difference ± SEM −1.0 ± 0.2 and −2.0 ± 0.2 mmol/L, respectively, P ≤ 0.0001, adj. P ≤ 0.0006), and combined FPG was lowered even further compared with placebo (−2.4 ± 0.2 mmol/L, P ≤ 0.0001, adj. P ≤ 0.0006) (Table 2 and Fig. 1A and B). The peak PG during the MMT was lowered significantly by empagliflozin, LY2409021, and the combination of the two (Table 2 and Fig. 1A). Empagliflozin and LY2409021 lowered peak PG similarly (P = 0.526), but the combination (empagliflozin + LY2409021) lowered peak PG significantly more than each compound alone (vs. empagliflozin P = 0.007 [adj. P = 0.020], vs. LY2409021 P < 0.0001 [adj. P < 0.001]) (Table 2 and Fig. 1A). Time to peak of PG was 103 ± 12 min for placebo and 100 ± 11 min for empagliflozin and tended to increase with LY2409021 (118 ± 11 min) and decrease with empagliflozin + LY2409021 (91 ± 10 min); however, all differences were insignificant. Compared with placebo, AUC was significantly lowered by empagliflozin (P < 0.001, adj. P < 0.001) and less convincingly by LY2409021 (P = 0.037, adj. P = 0.079), but AUCs during LY2409021 and empagliflozin were similar (P = 0.767) (Table 2 and Fig. 1A and C). The combination of empagliflozin + LY2409021 reduced AUC even further (Fig. 1A and C). The baseline-subtracted AUC (bsAUC) was significantly lower with empagliflozin compared with placebo, whereas LY2409021 significantly increased bsAUC (Table 2 and Fig. 1D), but when the agents were combined, empagliflozin eliminated the rise in bsAUC observed with LY2409021 (Table 2 and Fig. 1D).

      Table 2

      Summarized results

      Figure 1
      Figure 1

      Fasting and postprandial glucose concentrations. PG concentrations during liquid MMT (A), fasting PG concentrations (B), AUC (C), and bsAUC (D) on days with placebo, the SGLT2i empagliflozin (25 mg), the GRA (300 mg LY2409021), and the combination (GRA + SGLT2i) in patients with type 2 diabetes (N = 12). Data are mean ± SEM (symbols ± error bars) (A) and mean ± SEM (bars ± error bars) with individual values (symbols) (BD). Statistical comparisons were made with a linear mixed model, and P values illustrated are raw with P values adjusted for multiple comparisons by false discovery rate in parentheses. ns, not significant.

      Plasma Glucose Kinetics and Urine Excretion

      Empagliflozin alone (16.2 μmol × kg−1 × min−1) did not affect fasting EGP compared with placebo (16.8 μmol × kg−1 × min−1, P = 0.346), and adding empagliflozin to LY2409021 did not affect fasting EGP (13.6 μmol kg−1 × min−1) compared with LY2409021 alone (12.9 μmol kg−1 × min−1, P = 0.061, adj. P = 0.125) (Fig. 2E). In contrast, LY2409021 lowered fasting EGP compared with placebo and empagliflozin (both P < 0.0001, adj. P < 0.001), and the combination of empagliflozin + LY2409021 reduced fasting EGP compared with placebo and empagliflozin alone (both P < 0.001, adj. P < 0.01) (Fig. 2E). Postprandially, total glucose Ra was only affected (and reduced) by LY2409021 alone or in combination with empagliflozin, whereas empagliflozin alone did not affect glucose Ra (Fig. 2A and B). Glucose Rd was not reduced by empagliflozin, but LY2409021 and the combination of the two agents reduced Rd of glucose compared with placebo (Fig. 2G and H). Glucose excreted in the urine (Fig. 2J) and urine volume (Fig. 2I) were markedly increased on both empagliflozin days compared with placebo. Participants excreted a mean of 125 mmol (22.5 g) of glucose during the 2-h basal fasting plus 4-h postprandial experimental period with empagliflozin compared with 1.7 mmol (0.3 g) glucose with placebo (Fig. 2J). Urine glucose excretion was lower on the combination day (17.5 g glucose) compared with empagliflozin alone (Fig. 2J). The EGP during the 240 min was not changed by empagliflozin alone compared with placebo (Fig. 2E and F), but EGP was reduced by LY2409021 and empagliflozin + LY2409021 compared with placebo. When adding empagliflozin to LY2409021, EGP was increased compared with LY2409021 alone (Fig. 2E and F). Ra of the oral glucose tracer was similar on the 4 treatment days (Fig. 2C and D).

      Figure 2
      Figure 2

      Glucose kinetics and urinary glucose excretion. Ra of total glucose (A), oral glucose (C), EGP (E), and Rd of glucose (G) with summarized mmol of glucose appearing or disappearing during the 240-min MMT (B, D, F, and H); urine volume (I); and urine glucose excretion (J) in patients with type 2 diabetes (N = 12). Data are mean ± SEM (symbols ± error bars) (A, C, E, and G) and mean ± SEM (bars ± error bars) with individual values (symbols) (B, D, F, and HJ). Statistical comparisons were made with a linear mixed model, and P values illustrated are raw with P values adjusted for multiple comparisons by false discovery rate in parentheses. ns, not significant.

      Glucagon

      Compared with placebo, empagliflozin did not change fasting or postprandial plasma glucagon concentrations (Table 2 and Fig. 3A and B). In contrast, LY2409021 increased fasting plasma glucagon concentrations approximately threefold, and glucagon concentrations remained elevated throughout the MMT (Table 2 and Fig. 3A and B). Plasma glucagon concentrations during empagliflozin + LY2409021 were similar to glucagon concentrations during LY2409021 administration (Fig. 3A and B).

      Figure 3
      Figure 3

      Glucagon, C-peptide, and acetaminophen. Concentrations of glucagon (A), C-peptide (C), and acetaminophen (E) before and during the MMT in patients with type 2 diabetes (N = 12); data are mean ± SEM (symbols ± error bars). Summarized results as AUCs; data are mean ± SEM (bars ± error bars) with individual values (symbols) (B, D, and F). Statistical comparisons were made with a linear mixed model and P values illustrated are raw with P values adjusted for multiple comparisons by false discovery rate in parentheses. ns, not significant.

      C-Peptide and ISR

      LY2409021 and empagliflozin + LY2409021 significantly lowered fasting serum C-peptide concentrations compared with placebo and empagliflozin alone (Table 2 and Fig. 3C). Likewise, fasting ISR was reduced on all experimental days (insignificantly for empagliflozin) compared with placebo (Table 2). Postprandial excursions of C-peptide (AUC) were reduced compared with placebo by empagliflozin and empagliflozin + LY2409021 but were not affected by LY2409021 (Fig. 3D), whereas bsAUC of C-peptide was increased by LY2409021 compared with placebo and empagliflozin (Table 2 and Fig. 3D). Similarly, we observed a significant reduction of ISR AUC with empagliflozin + LY2409021 compared with placebo and LY2409021, and bsAUC of the ISR was increased with LY2409021 compared with placebo and empagliflozin (Table 2).

      Glycerol Concentrations and Kinetics

      During fasting conditions, empagliflozin + LY2409021 increased plasma glycerol concentration compared with placebo (P = 0.026, adj. P = 0.059) and empagliflozin alone (P = 0.0028, adj. P = 0.010). LY2409021 (P = 0.146) and empagliflozin (P = 0.652) alone did not affect fasting glycerol concentration significantly (Fig. 4A). Interindividual variation was high (Fig. 4A), and postprandial excursions of glycerol (AUC) differed only between empagliflozin versus empagliflozin + LY2409021 (P = 0.015, adj. P = 0.037) and LY2409021 versus empagliflozin + LY2409021 (P = 0.025, adj. P = 0.059). Fasting glycerol Ra (Fig. 4B), representing the whole-body lipolytic rate, was higher with empagliflozin + LY2409021 compared with placebo (P = 0.024, adj. P = 0.056), empagliflozin (P = 0.012, adj. P = 0.030), and LY2409021 (P = 0.006, adj. P = 0.018). Likewise, AUC for glycerol Ra showed a tendency to be higher with empagliflozin + LY2409021 compared with placebo (P = 0.133) and was significantly higher compared with empagliflozin (P = 0.006, adj. P = 0.016) and LY2409021 (P = 0.011, adj. P = 0.029).

      Figure 4
      Figure 4

      Glycerol concentrations and kinetics. Plasma glycerol concentrations during liquid MMT (A), Ra of glycerol (B), and Rd of glycerol (C) in patients with type 2 diabetes (N = 12). Data are mean ± SEM.

      Gastric Emptying, Energy Intake, and Energy Expenditure

      There were no differences in time to peak, peak acetaminophen concentration, or AUC of acetaminophen (proxy for gastric emptying) among any of the treatment days (Table 2 and Fig. 3E and F). Energy expenditure was measured before the MMT and 30 min after the MMT started, and we observed no differences in resting energy expenditure or respiratory quotient among any of the treatment days (Supplementary Table 1). The amount of food consumed (energy intake) during the ad libitum meal after time point 240 min did not differ among the 4 days (Supplementary Table 1).

      Discussion

      By subjecting patients with type 2 diabetes to MMTs preceded by single-dose administration of the SGLT2i empagliflozin, the GRA LY2409021, the combination empagliflozin + LY2409021, and double-dummy placebo, respectively, we report 1) no effects of empagliflozin on plasma glucagon concentrations or EGP, challenging previous findings; 2) modest and robust (subadditive) FPG-lowering effects of empagliflozin and LY2409021, respectively, through diverse mechanisms (empagliflozin through increased urinary glucose excretion and LY2409021 through reduced EGP); and 3) a paradoxically larger increment in postprandial glucose excursions with LY2409021, which was eliminated when LY2409021 was administered together with empagliflozin. To our knowledge, this study is the first to evaluate the effect of an SGLT2i combined with a GRA in humans. We found no effects of empagliflozin on plasma glucagon and EGP. In a previous study that included patients with type 2 diabetes (N = 66), Ferrannini et al. (10) showed that a single dose of empagliflozin (25 mg) increased EGP. The authors explained this phenomenon as a result of increased glucagon concentrations and decreased insulin secretion after a MMT. In contrast, we observe no impact of empagliflozin (the same dose) on plasma glucagon concentrations or fasting or postprandial EGP. Nevertheless, we found that acute induction of glucosuria by empagliflozin leads to reductions in fasting and postprandial C-peptide concentrations, which is in agreement with the findings of Ferrannini et al. Differences between the studies may contribute to the explanation for the different observations related to glucagon and EGP. In our study, the labeled glucose in the liquid meal was dissolved in the total content of the meal, whereas the white bread–derived carbohydrates in the solid meal was imputed to calculate EGP by Ferrannini et al. In contrast to Ferrannini et al., who administered empagliflozin nonblinded 3.5 h before the meal test, we administered empagliflozin 2 h before the MMT in a double-blinded fashion. The timing of empagliflozin dosing was based on pharmacokinetic properties of the compound demonstrating Cmax for empagliflozin after 1–2 h (45), which is supported by the clear effects on urinary glucose excretion and the ensuing reductions in FPG and postprandial PG concentrations. Studying dapagliflozin-induced glucosuria in men with diabetes (n = 12 dapagliflozin, n = 6 placebo), Merovci et al. (11) found increased basal EGP (using a stable infusion of [3-3H]glucose) together with increased plasma glucagon concentrations 4 h after administration. Given the tendency of increased glucagon concentrations that we observed with empagliflozin after 2 h, we cannot completely exclude that we could have found a greater increase 3 or 4 h postdose as in the abovementioned studies. Thus, our data do not reproduce the findings of Ferrannini et al. and Merovci et al. with regard to increased glucagon concentrations and EGP after single doses of empagliflozin and dapagliflozin, respectively. In fact, we observed that EGP is larger with empagliflozin + LY2409021 compared with LY2409021 alone, suggesting that glucagon cannot explain the difference in EGP (glucagon receptors are blocked). We cannot rule out problems of sample size and type II errors with the limited number of participants (N = 12) in our study. However, a few other studies have reported similar glucagon data to ours with glucagon measured by Mercodia ELISA (46,47). The latter studies and ours have reported lower glucagon concentrations compared with those of Merovci et al. and Ferrannini et al., suggesting that differences in glucagon assays used may explain some of the differences in absolute concentrations of glucagon measured. The radioimmunoassay used in this study has been validated against mass spectrophotometry (39). Differences in glucagon assays might possibly explain a difference between ours and findings by others if, for example, SGLT2 inhibition by some unknown mechanism increases glucagon-like peptides and/or glucagon precursor sequences but not glucagon (3361) itself. Increases in glucagon concentrations after SGLT2i treatment have been explained by direct stimulation of SGLT2 on α-cells, but recent data demonstrated large variability in SGLT2i effect on glucagon secretion in human islets (48), and direct effects on α-cells are still debated (15,16). In light of these new findings, it may not be surprising that empagliflozin did not increase glucagon concentrations in this study. Moreover, varying baseline glucose levels may play a role in glucagon secretion (49), and a higher glucagon-to-insulin ratio seems to be associated with poor glycemic control (50). New data have indicated that glucagon concentrations during acute SGLT2i treatment are mainly mediated through glycemic changes and that a direct effect on α-cells is of less importance (46); this is in line with higher (insignificant) fasting glucagon concentrations with LY2409021 + empagliflozin, where glucose concentration is lower compared with LY2409201. Previous studies indicated that longer-term treatment with empagliflozin and dapagliflozin may blunt the suggested increases in EGP and glucagon concentrations (10,11); however, we were able to look at the acute effects of single doses only. Given the phenotype of our participants with type 2 diabetes (high total glucose), a longer tracer equilibrium period (e.g., of 180 min) might have been desirable during baseline.

      We found no rise in EGP and glucagon concentrations with empagliflozin in this study but, nevertheless, observed a clinically relevant, subadditive reduction of FPG with the combination of empagliflozin + LY2409021 compared with the effects of LY2409021 and empagliflozin alone. Glucagon receptor antagonism is particularly efficient in lowering fasting and premeal glucose concentrations (5154). With the double-tracer technique, we confirmed that FPG is reduced with LY2409021 as a result of reduction of fasting EGP. Empagliflozin and other SGLT2i exert their glucose-lowering effect by inducing glucosuria. In normal physiology, ∼180 g of glucose is filtered through the glomeruli during 24 h, but all glucose is reabsorbed through SGLT-dependent mechanisms, so no glucose is excreted in healthy individuals (55). However, when glucose reabsorptive mechanisms are saturated above a threshold of ∼11 mmol/L, glucose is excreted in a linear manner with increasing PG concentration (55). Patients with type 2 diabetes have increased expression and activity of SGLT2 (56), and thus, inhibition of renal glucose reabsorption with a single dose of 25 mg empagliflozin has previously been shown to result in a glucose excretion of 60–90 g per 24 h in these patients (57,58). This is in line with our results; we observed 22.5 g glucose excreted during the 6-h experimental day (fasting and prandial conditions). During the empagliflozin + LY2409021 day, we observed lower urinary excretion of glucose (17.5 g glucose per 6 h), which we ascribe to the lower PG concentrations on that day.

      We report a paradoxically large increment in postprandial glucose excursions with LY2409021. Previous studies have been inconsistent in the effect of GRA on postprandial glucose excursions (51,52). We believe that this can be explained by cross-reactivity and inhibition of the glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 receptor because of the high theoretical concentration of LY2409021 achieved with the dose of 300 mg. We have investigated the in vitro inhibitory effect of LY2409021 on the GIP and GLP-1 receptors (data not published), and on the basis of previous concentration-versus-time profiles (30), we estimate that with the dose of 300 mg, ∼50–80% of GIP and GLP-1 receptor activity may be inhibited. Another possible explanation of the paradoxical increment in postprandial glucose excursions with LY2409021 could be diminished disappearance of glucose (lower Rd as seen in Fig. 2H) secondary to decreased glucose levels and, thereby, decreased glucose-mediated transport through GLUT-4 in muscle cells (59). SGLT2 inhibition lowers glucose excursions after an oral glucose tolerance test (58), and canagliflozin has shown a near 50% greater reduction of postmeal glucose compared with reduction of FPG (60) (possibly as a result of canagliflozin’s low-potency SGLT1 inhibition delaying intestinal glucose absorption as well) (4). We report a reduction of both AUC and bsAUC of glucose after a single dose of empagliflozin, which was due to increased urinary glucose excretion without any effect on EGP. Our data illustrate the efficient glucose-lowering combination of reduced fasting EGP with glucagon receptor antagonism and the postprandial glucose-lowering effect of an SGLT2i (reduction of urinary glucose excretion threshold).

      SGLT2i have been associated with increased ketogenesis and a shift from glucose oxidation to hepatic fat oxidation. The mechanism has previously been explained by the possible connection to increased glucagon concentrations; however, recently, SGLT2i-induced ketosis has been shown to be independent of glucagon and insulin, suggesting that a complementary ketogenic factor is involved in SGLT2i-induced ketosis (61). The lack of increased glucagon concentrations with empagliflozin and the limited effect of glucagon on the glucose-lowering effect of empagliflozin in the current study support this hypothesis. There is no evidence that glucagon affects peripheral lipolysis in human physiology (62), but SGLT2i increases the concentration of nonesterified fatty acids (61). Here, we report no significant effect of LY2409021 and empagliflozin on the fasting glycerol concentration, but the combination of the two treatments increased fasting glycerol and postprandial AUC. The lack of significant results may represent type II errors. Insulin strongly inhibits peripheral lipolysis and thereby the supply of nonesterified fatty acids, and we believe that our glycerol results may reflect the lower insulin levels with empagliflozin + LY2409021 (lower insulin-mediated inhibition of lipolysis).

      In the current study, we had a unique opportunity, as an exploratory, secondary end point, to investigate the combined effects of single dosing of a GRA and an SGLT2i on food intake and energy expenditure. SGLT2i promote a significant body weight loss through sustained glucose (energy) loss through the urine (4). SGLT2i-induced body weight loss could alternatively be caused by increased energy expenditure or decreased energy intake, but longer-term clinical trials with canagliflozin (52-week phase III) showed an initial period of body weight loss followed by a body weight plateau because of a compensatory increase in energy intake to match the calories lost in urine (63) without any effects on energy expenditure (10,63). Exogenous glucagon has been shown to decrease food intake by inducing satiety (64), but the effects of GRA on food intake and energy expenditure have not previously been reported. Here, we report no differences in ad libitum food intake after a single dose of LY2409021 and empagliflozin, individually or combined. Moreover, we confirmed previous findings of no effects on energy expenditure during acute administration of an SGLT2i (10,63).

      In conclusion, in contrast to previous studies, we found that a single (clinically recommended) dose of empagliflozin increased neither glucagon concentrations nor EGP in patients with type 2 diabetes. Nevertheless, we found that the combination of the SGLT2i empagliflozin and the GRA LY2409021 reduced FPG beyond their individual capacity in patients with type 2 diabetes. Glucagon receptor antagonism resulted in a paradoxically increased increment in postprandial baseline-corrected glucose excursions, which was eliminated by the empagliflozin-induced glucosuria. Taken together, our findings suggest that circulating glucagon levels do not limit the glucose-lowering effect of a single dose of empagliflozin in patients with type 2 diabetes.

      Article Information

      Acknowledgments. The authors thank Sisse Schmidt (Gentofte Hospital), Inass Nachar (Gentofte Hospital), and Lene Albæk (University of Copenhagen) for laboratory assistance and Julie L. Forman (University of Copenhagen) for statistical expertise and support.

      Funding. The study was funded by the Danish Diabetes Academy supported by the Novo Nordisk Foundation and the A.P. Møller Fonden til Lӕgevidenskabens Fremme.

      Duality of Interest. A.L. has received lecture fees from Novo Nordisk and AstraZeneca. J.J.H. is currently receiving speaker honoraria from Novo Nordisk and MSD and is on advisory boards for Novo Nordisk. F.K.K. has served on scientific advisory panels and/or been part of speakers’ bureaus for, served as a consultant to, and/or received research support from Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Carmot Therapeutics, Eli Lilly, Gubra, MedImmune, MSD/Merck, Mundipharma, Norgine, Novo Nordisk, Sanofi, and Zealand Pharma. T.V. has served on scientific advisory panels, been part of speakers’ bureaus for, served as a consultant to, and/or received research support from Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Gilead Sciences, Mundipharma, MSD/Merck, Novo Nordisk, Sanofi, and Sun Pharmaceuticals. No other potential conflicts of interest relevant to this article were reported.

      Author Contributions. S.H., A.L., F.K.K., and T.V. designed the study, wrote the study protocol, and wrote the manuscript. S.H., E.N.-H., and H.M. performed the study. G.v.H. and J.J.H. generated and interpreted data. All authors critically edited the manuscript and approved the final version. S.H. and T.V. are the guarantors of this work and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

      Prior Presentation. Parts of this study were presented in abstract form at the 78th Scientific Sessions of the American Diabetes Association, Orlando, FL, 22–26 June 2018, and at the 54th Annual Meeting of the European Association for the Study of Diabetes, Berlin, Germany, 1–5 October 2018.

      • Received April 10, 2020.
      • Accepted September 24, 2020.



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      Crustless Quiche with Italian Turkey Sausage and Peppers

      By electricdiet / January 31, 2021


      This crustless quiche with Italian turkey sausage and peppers is bursting with delicious flavor! It’s a great make-ahead breakfast to enjoy all week.

      Crustless Quiche with Italian Turkey Sausage and Peppers in a baking dish with one slice removed to a plate

      Quiches are such a great make-ahead breakfast. They’re perfect for brunch with friends, a family gathering, or simply to meal-prep for the week.

      And when you want a hearty dish that won’t leave you feeling heavy and exhausted for hours after, you have to try this crustless quiche with Italian turkey sausage and peppers!

      By ditching the crust, this quiche becomes a high-protein and low-carb breakfast that’s perfect for starting your day. You’ll have energy for hours without the crash.

      And thanks to the turkey sausage and peppers, it’s absolutely bursting with delicious flavor, too!

      How to make crustless quiche with Italian turkey sausage and peppers

      This tasty quiche is simple to prep and uses less than 10 ingredients!

      Step 1: Preheat the oven to 375°F.

      Step 2: Spray a 9-inch pie plate with nonstick cooking spray. Sprinkle the bread crumbs into the bottom of the pie plate.

      Step 3: In a large skillet, cook the crumbled turkey sausage and onions over medium-high heat, stirring occasionally, for about 7 minutes. Once the meat is no longer pink and the onions are translucent, transfer to a plate lined with paper towels to drain.

      Step 4: Add the sausage and onions to the pie plate, distributing evenly.

      Step 5: Sprinkle the pie plate with the green pepper, red pepper, and cheese.

      Step 6: In a medium bowl, whisk together the eggs, milk, and pepper, then pour into the pie plate.

      Step 7: Place in the oven and bake for 35 to 40 minutes or until the center is set and the top is beginning to brown in spots.

      Step 8: Remove from the oven and set the pie plate on a wire rack. Allow to cool for about 10 minutes before slicing into wedges.

      Enjoy your tasty quiche for a nutritious breakfast, quick lunch, or even a delicious dinner! After all, there’s no reason you should only get to eat eggs for breakfast.

      Variations for this recipe

      There are so many different ways to make quiches. If you want, you can use this recipe as a base and modify based on your tastes and preferences!

      Looking for a gluten-free option? Just use gluten-free bread crumbs and make sure your turkey sausage is gluten-free as well. Want to reduce the fat and cholesterol? Use 1 cup of egg substitute instead of whole eggs.

      You can also play around with the flavors and ingredients. Instead of turkey sausage, you could try turkey bacon, cubed ham, or even pulled chicken. Swap the bell peppers out for other crunchy veggies (or just add more vegetables!)

      Don’t have mozzarella on hand? Use whatever cheese is in your fridge! If you ask me, it’s hard to go wrong with cheese.

      Storage

      Once your quiche has fully cooled, you can store it covered in the refrigerator for up to 5 days. If you try to cover it while it’s still warm, you may end up with condensation that will make your quiche soggy.

      Leftovers reheat very well in the microwave, so you can enjoy them at home or just as easily take them on-the-go!

      Quiche in a red dish on a wooden table

      Other make-ahead breakfast recipes

      If you’re like me, you don’t always have time to prep a nice and healthy breakfast in the morning. But I firmly believe that what we eat the morning sets the tone for the rest of the day. So here are a few of my favorite make-ahead breakfasts to start my day the right way:

      When you’ve tried this quiche, please don’t forget to let me know how you liked it and rate the recipe in the comments below!

      Recipe Card

      Crustless Quiche with Italian Turkey Sausage and Peppers in a baking dish with one slice removed to a plate

      Crustless Quiche with Italian Turkey Sausage and Peppers

      This crustless quiche with Italian turkey sausage and peppers is bursting with delicious flavor! It’s a great make-ahead breakfast to enjoy all week.

      Prep Time:5 minutes

      Cook Time:45 minutes

      Total Time:50 minutes

      Author:Shelby Kinnaird

      Servings:8

      Instructions

      • Preheat the oven to 375°F.

      • Spray a 9-inch pie plate with nonstick cooking spray. Sprinkle the bread crumbs into the bottom of the pie plate.

      • In a large skillet, cook the crumbled turkey sausage and onions over medium-high heat, stirring occasionally, for about 7 minutes. Once the meat is no longer pink and the onions are translucent, transfer to a plate lined with paper towels to drain.

      • Add the sausage and onions to the pie plate, distributing evenly.

      • Sprinkle the pie plate with the green pepper, red pepper, and cheese.

      • In a medium bowl, whisk together the eggs, milk, and pepper, then pour into the pie plate.

      • Place in the oven and bake for 35 to 40 minutes or until the center is set and the top is beginning to brown in spots.

      • Remove from the oven and set the pie plate on a wire rack. Allow to cool for about 10 minutes before slicing into wedges.

      Recipe Notes

      This recipe is for 8 servings. If you cut the quiche into 8 slices, each serving will be 1 slice.
      For a gluten-free recipe, use gluten-free bread crumbs and turkey sausage.
      To reduce the fat and cholesterol, use 1 cup egg substitute instead of the whole eggs.
      Leftovers can be stored covered in the refrigerator for up to 5 days.

      Nutrition Info Per Serving

      Nutrition Facts

      Crustless Quiche with Italian Turkey Sausage and Peppers

      Amount Per Serving (1 slice)

      Calories 135
      Calories from Fat 63

      % Daily Value*

      Fat 7g11%

      Saturated Fat 3g19%

      Trans Fat 0g

      Polyunsaturated Fat 1g

      Monounsaturated Fat 1g

      Cholesterol 120mg40%

      Sodium 496mg22%

      Potassium 186mg5%

      Carbohydrates 5g2%

      Fiber 1g4%

      Sugar 3g3%

      Protein 12g24%

      Net carbs 4g

      * Percent Daily Values are based on a 2000 calorie diet.

      Course: Breakfast

      Cuisine: American

      Diet: Diabetic, Gluten Free

      Keyword: crustless quiche, easy breakfast recipes



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      Mini Banana Bread Loaves –

      By electricdiet / January 29, 2021





      Mini Banana Bread Loaves –



































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