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Diabetic Ketoacidosis In Dogs

Diabetic Ketoacidosis In Dogs

My dog is diabetic. He has been doing pretty well overall, but recently he became really ill. He stopped eating well, started drinking lots of water, and got really weak. His veterinarian said that he had a condition called “ketoacidosis,” and he had to spend several days in the hospital. I’m not sure I understand this disorder. Diabetic ketoacidosis is a medical emergency that occurs when there is not enough insulin in the body to control blood sugar (glucose) levels. The body can’t use glucose properly without insulin, so blood glucose levels get very high, and the body creates ketone bodies as an emergency fuel source. When these are broken down, it creates byproducts that cause the body’s acid/base balance to shift, and the body becomes more acidic (acidosis), and it can’t maintain appropriate fluid balance. The electrolyte (mineral) balance becomes disrupted which can lead to abnormal heart rhythms and abnormal muscle function. If left untreated, diabetic ketoacidosis is fatal. How could this disorder have happened? If a diabetic dog undergoes a stress event of some kind, the body secretes stress hormones that interfere with appropriate insulin activity. Examples of stress events that can lead to diabetic ketoacidosis include infection, inflammation, and heart disease. What are the signs of diabetic ketoacidosis? The signs of diabetic ketoacidosis include: Excessive thirst/drinking Increased urination Lethargy Weakness Vomiting Increased respiratory rate Decreased appetite Weight loss (unplanned) with muscle wasting Dehydration Unkempt haircoat These same clinical signs can occur with other medical conditions, so it is important for your veterinarian to perform appropriate diagnostic tests to determine if diabetic ketoacidosis in truly the issue at hand Continue reading >>

Can An Add-on Pill For Type 1 Diabetes Improve A1c And Weight Loss?

Can An Add-on Pill For Type 1 Diabetes Improve A1c And Weight Loss?

Trial results testing sotagliflozin and Farxiga in type 1 diabetes show greater A1c lowering and weight loss, plus continued conversation about small risk of DKA Potential “add-on” (adjunctive) treatments for type 1 diabetes played a starring role at the 2017 EASD conference. Key trial results were announced for two non-insulin drugs that come in pill form, offering people with type 1 diabetes an exciting new option to manage blood sugars. The DEPICT 1 examined the use of Farxiga, a once-daily pill (an SGLT-2 inhibitor) currently approved for treating type 2 diabetes but not type 1, while the inTandem3 study tested an SGLT-1/2 dual inhibitor, sotagliflozin, also a once-daily pill that has not yet been approved. While these studies are not meant to be compared to each other given the general lack of standardization in the world of trial design, they both add to the excitement about the possibility of adjunct therapies for people with type 1. Both studies reported A1c reductions and weight loss – great for the push to approve add-on therapies for type 1 – along with continued discussion about diabetic ketoacidosis (DKA). With these phase 3 trial results, the companies may now choose to submit the drugs to the FDA and pursue an “indication” for use in type 1 diabetes. The pills are taken once daily and work independent of insulin, meaning they won’t require complicated dosing. Glucose is only excreted through the urine when blood sugars are high, and then the drugs stop working when glucose levels come down. Read more below! Jump to a section: DEPICT 1 DEPICT 1 followed 833 participants with type 1 diabetes for 24 weeks; on average, they had an A1c of 8.5% and a daily insulin dose of 60 units. In addition to their regular insulin therapy, study participants e Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Amphetamine-like Analogues In Diabetes: Speeding Towards Ketogenesis

Amphetamine-like Analogues In Diabetes: Speeding Towards Ketogenesis

Case Reports in Endocrinology Volume 2015 (2015), Article ID 917869, 4 pages Division of Endocrinology, Diabetes and Metabolism, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, P.O. Box 693, Rochester, NY 14642, USA Academic Editor: Toshihiro Kita Copyright © 2015 Natalia M. Branis and Steven D. Wittlin. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Obesity is common in patients with type 1 and type 2 diabetes. Amphetamine-like analogues comprise the most popular class of weight loss medications. We present a case of a 34-year-old African American female with a history of type 1 diabetes, dyslipidemia, and obesity who developed diabetic ketoacidosis (DKA) after starting Diethylpropion for the purpose of weight loss. Shortly after starting Diethylpropion, she developed nausea, vomiting, and periumbilical pain. Blood work revealed glucose of 718 mg/dL, pH 7.32 (7.35–7.45), bicarbonate 16 mmol/L (22–29 mmol/L), and anion gap 19 mmol/L (8–16 mmol/L). Urine analysis demonstrated large amount of ketones. She was hospitalized and successfully treated for DKA. Diethylpropion was discontinued. Amphetamine-like analogues administration leads to norepinephrine release from the lateral hypothalamus which results in the appetite suppression. Peripheral norepinephrine concentration rises as well. Norepinephrine stimulates adipocyte lipolysis and thereby increases nonesterified fatty acids (NEFA) availability. It promotes β-oxidation of NEFA to ketone bodies while decreasing metabolic clearance rate of ketones. In the setting of acute insulin deficiency these effects ar Continue reading >>

> Hyperglycemia And Diabetic Ketoacidosis

> Hyperglycemia And Diabetic Ketoacidosis

When blood glucose levels (also called blood sugar levels) are too high, it's called hyperglycemia. Glucose is a sugar that comes from foods, and is formed and stored inside the body. It's the main source of energy for the body's cells and is carried to each through the bloodstream. But even though we need glucose for energy, too much glucose in the blood can be unhealthy. Hyperglycemia is the hallmark of diabetes — it happens when the body either can't make insulin (type 1 diabetes) or can't respond to insulin properly (type 2 diabetes). The body needs insulin so glucose in the blood can enter the cells to be used for energy. In people who have developed diabetes, glucose builds up in the blood, resulting in hyperglycemia. If it's not treated, hyperglycemia can cause serious health problems. Too much sugar in the bloodstream for long periods of time can damage the vessels that supply blood to vital organs. And, too much sugar in the bloodstream can cause other types of damage to body tissues, which can increase the risk of heart disease and stroke, kidney disease, vision problems, and nerve problems in people with diabetes. These problems don't usually show up in kids or teens with diabetes who have had the disease for only a few years. However, they can happen in adulthood in some people, particularly if they haven't managed or controlled their diabetes properly. Blood sugar levels are considered high when they're above someone's target range. The diabetes health care team will let you know what your child's target blood sugar levels are, which will vary based on factors like your child's age. A major goal in controlling diabetes is to keep blood sugar levels as close to the desired range as possible. It's a three-way balancing act of: diabetes medicines (such as in Continue reading >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Diabetic Ketoacidosis: A Challenging Diabetes Phenotype

Diabetic Ketoacidosis: A Challenging Diabetes Phenotype

HRB Clinical Research Facility, Galway University Hospitals, National University of Ireland, Galway Ireland Summary We describe three patients presenting with diabetic ketoacidosis secondary to ketosis prone type 2, rather than type 1 diabetes. All patients were treated according to a standard DKA protocol, but were subsequently able to come off insulin therapy while maintaining good glycaemic control. Ketosis-prone type 2 diabetes (KPD) presenting with DKA has not been described previously in Irish patients. The absence of islet autoimmunity and evidence of endogenous beta cell function after resolution of DKA are well-established markers of KPD, but are not readily available in the acute setting. Although not emphasised in any current guidelines, we have found that a strong family history of type 2 diabetes and the presence of cutaneous markers of insulin resistance are strongly suggestive of KPD. These could be emphasised in future clinical practice guidelines. Learning points: Even in white patients, DKA is not synonymous with type 1 diabetes and autoimmune beta cell failure. KPD needs to be considered in all patients presenting with DKA, even though it will not influence their initial treatment. Aside from markers of endogenous beta cell function and islet autoimmunity, which in any case are unlikely to be immediately available to clinicians, consideration of family history of type 2 diabetes and cutaneous markers of insulin resistance might help to identify those with KPD and are more readily apparent in the acute setting, though not emphasised in guidelines. Consideration of KPD should never alter the management of the acute severe metabolic derangement of DKA, and phasing out of insulin therapy requires frequent attendance and meticulous and cautious surveillanc Continue reading >>

Sglt2 Inhibitors: Updated Advice On The Risk Of Diabetic Ketoacidosis

Sglt2 Inhibitors: Updated Advice On The Risk Of Diabetic Ketoacidosis

Advice for healthcare professionals: When treating patients who are taking a sodium-glucose co-transporter 2 (SGLT2) inhibitor (canagliflozin, dapagliflozin, or empagliflozin): inform them of the signs and symptoms of diabetic ketoacidosis (DKA) – see below – and advise them to seek immediate medical advice if they develop any of these discuss the risk factors for DKA with patients (see below) discontinue treatment with the SGLT2 inhibitor immediately if DKA is suspected or diagnosed do not restart treatment with any SGLT2 inhibitor in patients who experienced DKA during use, unless another cause for DKA was identified and resolved interrupt treatment with the SGLT2 inhibitor in patients who are hospitalised for major surgery or acute serious illnesses; treatment may be restarted once the patient’s condition has stabilised Reports of diabetic acidosis EU medicines regulators have completed a review of DKA associated with SGLT2 inhibitor treatment; this article summarises the review’s recommendations. We published preliminary advice on this in June 2015. SGLT2 inhibitors are licensed for use in adults with type 2 diabetes to improve glycaemic control. Serious, life-threatening, and fatal cases of DKA have been reported in patients taking an SGLT2 inhibitor (canagliflozin, dapagliflozin, or empagliflozin). The EU review concluded that this side effect is rare (affecting between 1 in 1000 and 1 in 10,000 patients). Up to 26 February 2016, we had received 118 Yellow Card reports of DKA and associated reactions in patients taking an SGLT2 inhibitor in the UK. In several cases, blood glucose levels were only moderately elevated (eg <14mmol/L)—representing an atypical presentation for DKA, which could delay diagnosis and treatment. Therefore inform patients of the si Continue reading >>

Is Ketosis Dangerous?

Is Ketosis Dangerous?

You may have heard from your doctor that ketosis is a life-threatening condition. If so, your doctor is confusing diabetic ketoacidosis (DKA) with nutritional ketosis, or keto-adaptation. First, some semantics. Our body can produce, from fat and some amino acids, three ketone bodies (a “ketone” refers to the chemical structure where oxygen is double-bonded to carbon sandwiched between at least 2 other carbons). These ketone bodies we produce are: acetone, acetoacetone, and beta-hydroxybutyrate (B-OHB). [For anyone who is interested, they are the 3 most right structures on the figure, below.] Why do we make ketones? For starters, it’s a vital evolutionary advantage. Our brain can only function with glucose and ketones. Since we can’t store more than about 24 hours’ worth of glucose, we would all die of hypoglycemia if ever forced to fast for more than a day. Fortunately, our liver can take fat and select amino acids (the building blocks of proteins) and turn them into ketones, first and foremost to feed our brains. Hence, our body’s ability to produce ketones is required for basic survival. What is diabetic ketoacidosis? When diabetics (usually Type I diabetics, but sometimes this occurs in very late-stage, insulin-dependent, Type II diabetics) fail to receive enough insulin, they go into an effective state of starvation. While they may have all the glucose in the world in their bloodstream, without insulin, they can’t get any into their cells. Hence, they are effectively going into starvation. The body does what it would do in anyone – it starts to make ketones out of fat and proteins. Here’s the problem: the diabetic patient in this case can’t produce any insulin, so there is no feedback loop and they continue to produce more and more ketones withou Continue reading >>

Does The Ketogenic Diet Work For Type 2 Diabetes?

Does The Ketogenic Diet Work For Type 2 Diabetes?

You’ve probably seen dozens of headlines about the ketogenic diet by now, which has made its way into popular culture largely by celebrities and supermodels giving the long-standing fad diet a repeated stamp of approval. Is this the diet to follow if you have diabetes? Studies suggest the answer isn’t so simple. Some science shows its meal plan may be helpful, while other research, like one study published in September 2016 in Nutrients, highlights the importance of whole grains in the diets of people with diabetes — a restricted food category in the ketogenic diet. While the keto diet can offer many potential benefits for diabetes management, following it requires pretty serious commitment. So take a beat before you take the plunge — and consider these questions that can help you and your medical team determine if it’s right for you: How Does the Ketogenic Diet Work Exactly? There’s a good reason the ketogenic diet is also referred to as a low-carb, high-fat diet. Indeed, following the ketogenic diet means reducing carbohydrate intake to typically less than 50 grams (g) of carbohydrates per day, while increasing fat and protein intake, according to a review published in August 2013 in the European Journal of Clinical Nutrition. To put that into perspective, an individual on an average, non-restricted diet can easily eat more carbohydrates than that in one typical meal — for instance, a turkey, cheese, and veggie sandwich on whole-grain bread with a small, 1 ounce (oz) bag of classic potato chips would come in at around 51 g of carbs. These dietary changes drive down insulin levels, eventually leading your body into a state of ketosis, during which it is burning fat rather than carbohydrates. What Are Some of the Potential Benefits of a Ketogenic Diet for Continue reading >>

Diabetes Complications In Dogs And Cats: Diabetes Ketoacidosis (dka)

Diabetes Complications In Dogs And Cats: Diabetes Ketoacidosis (dka)

Unfortunately, we veterinarians are seeing an increased prevalence of diabetes mellitus in dogs and cats. This is likely due to the growing prevalence of obesity (secondary to inactive lifestyle, a high carbohydrate diet, lack of exercise, etc.). So, if you just had a dog or cat diagnosed with diabetes mellitus, what do you do? First, we encourage you to take a look at these articles for an explanation of the disease: Diabetes Mellitus (Sugar Diabetes) in Dogs Once you have a basic understanding of diabetes mellitus (or if you already had one), this article will teach you about life-threatening complications that can occur as a result of the disease; specifically, I discuss a life-threatening condition called diabetes ketoacidosis (DKA) so that you know how to help prevent it! What is DKA? When diabetes goes undiagnosed, or when it is difficult to control or regulate, the complication of DKA can occur. DKA develops because the body is so lacking in insulin that the sugar can’t get into the cells -- resulting in cell starvation. Cell starvation causes the body to start breaking down fat in an attempt to provide energy (or a fuel source) to the body. Unfortunately, these fat breakdown products, called “ketones,” are also poisonous to the body. Symptoms of DKA Clinical signs of DKA include the following: Weakness Not moving (in cats, hanging out by the water bowl) Not eating to complete anorexia Large urinary clumps in the litter box (my guideline? If it’s bigger than a tennis ball, it’s abnormal) Weight loss (most commonly over the back), despite an overweight body condition Excessively dry or oily skin coat Abnormal breath (typically a sweet “ketotic” odor) In severe cases DKA can also result in more significant signs: Abnormal breathing pattern Jaundice Ab Continue reading >>

Is Keto Healthy? Ketosis Vs Ketoacidosis

Is Keto Healthy? Ketosis Vs Ketoacidosis

Is Keto Healthy? Ketosis vs Ketoacidosis When looking at a ketogenic diet and ketosis, it’s common for some people to confuse the process with a harmful, more extreme version of this state known as diabetic ketoacidosis. But there are a lot of misconceptions out there about ketosis vs ketoacidosis, and it’s time to shed some light on the subject by looking at the (very big) differences between the two. An Overview of Ketosis A ketogenic, or keto, diet is centered around the process of ketosis, so it’s important to understand exactly what ketosis is first before we get into whether or not it’s safe (spoiler: it is): Ketosis is a metabolic state where the body is primarily using fat for energy instead of carbohydrates. Burning carbohydrates (glucose) for energy is the default function of the body, so if glucose is available, the body will use that first. But during ketosis, the body is using ketones instead of glucose. This is an amazing survival adaptation by the body for handling periods of famine or fasting, extreme exercise, or anything else that leaves the body without enough glucose for fuel. Those eating a ketogenic diet purposely limit their carb intake (usually between 20 and 50 grams per day) to facilitate this response. That’s why the keto diet focuses on very low carb intake, moderate to low protein intake, and high intakes of dietary fats. Lower protein is important because it prevents the body from pulling your lean muscle mass for energy and instead turns to fat. Ketone bodies are released during ketosis and are created by the liver from fatty acids. These ketones are then used by the body to power all of its biggest organs, including the brain, and they have many benefits for the body we’ll get into later. But first, let’s address a common mi Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Craig Cocchio, PharmD, BCPS, is an Emergency Medicine Clinical Pharmacist at Trinity Mother Frances Hospital in Tyler, Texas. Follow on Twitter @iEMPharmD and on his blog at empharmd.blogspot.com Diabetic ketoacidosis (DKA) in patients with presenting serum blood glucose <200 mg/dL isn’t common. More often, it’s seen in patients with type 1 diabetes in conjunction with starvation and acute illness.1 It’s difficult to determine an incidence of euglycemic DKA (euDKA) among all DKA cases in the literature, given the migration of the serum glucose cutoff from ≤300 mg/dL to ≤200 mg/dL. The best estimation based on an analysis of case reports suggests an incidence anywhere between 0.8% and 7.5%.1 However, the sodium-glucose cotransporter-2 (SGLT2) inhibitors canagliflozin, dapagliflozin, and empagliflozin can apparently induce this once-rare form of DKA.2,3 SGLT2 inhibitors are a class of oral hypoglycemic drugs indicated only for type 2 diabetes. Their novel mechanism of action prevents glucose reabsorption from the proximal renal tubules, resulting in increased glucosuria and decreasing plasma glucose. SGLT2 inhibitors lower serum glucose and HBA1C levels, and even produce weight loss. However, the increased glucose concentration in the bladder is a terrific incubation environment for fungi and bacteria, so much so that the FDA stuck a post-marketing warning on the drug class for the increased risk of serious urinary tract infections and urosepsis, in addition to euglycemic DKA. The proposed mechanism suggests that while SGLT2 inhibitors lower serum glucose, they also reduce insulin secretion from pancreatic beta cells in a negative feedback fashion. The lower serum insulin coupled with lower serum glucose consequently shifts energy metabolism to antilipolytic act Continue reading >>

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