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Diabetes Catabolic State

Type 1 Diabetes Mellitusclinical Presentation

Type 1 Diabetes Mellitusclinical Presentation

Type 1 Diabetes MellitusClinical Presentation Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD more... The most common symptoms of type 1 diabetes mellitus (DM) are polyuria, polydipsia, and polyphagia, along with lassitude, nausea, and blurred vision, all of which result from the hyperglycemia itself. Polyuria is caused by osmotic diuresis secondary to hyperglycemia. Severe nocturnal enuresis secondary to polyuria can be an indication of onset of diabetes in young children. Thirst is a response to the hyperosmolar state and dehydration. Fatigue and weakness may be caused by muscle wasting from the catabolic state of insulin deficiency, hypovolemia, and hypokalemia. Muscle cramps are caused by electrolyte imbalance. Blurred vision results from the effect of the hyperosmolar state on the lens and vitreous humor. Glucose and its metabolites cause osmotic swelling of the lens, altering its normal focal length. Symptoms at the time of the first clinical presentation can usually be traced back several days to several weeks. However, beta-cell destruction may have started months, or even years, before the onset of clinical symptoms. The onset of symptomatic disease may be sudden. It is not unusual for patients with type 1 DM to present with diabetic ketoacidosis (DKA), which may occur de novo or secondary to the stress of illness or surgery. An explosive onset of symptoms in a young lean patient with ketoacidosis always has been considered diagnostic of type 1 DM. Over time, patients with new-onset type 1 DM will lose weight, despite normal or increased appetite, because of depletion of water and a catabolic state with reduced glycogen, proteins, and triglycerides. Weight loss may not occur if treatment is initiated promptly after the onset of the Continue reading >>

An Integrated Approach To Diabetic Retinopathy Research

An Integrated Approach To Diabetic Retinopathy Research

Overview of anabolic insulin actions. A, Insulin binds to its receptor on the cell surface, leading to anabolic processes via activation of a cascade of intermediate proteins and enzymes that enable use of nutrients for energy or conversion to macromolecules. B, Insulin deficiency and/or insulin resistance creates a catabolic state with accelerated breakdown of macromolecules and accumulation of nutrients (glucose, amino acids, and free fatty acids) in the plasma. MAPK indicates mitogen-activated protein kinase. Insulin deficiency affects multiple tissues. A, A patient in 1922 with type 1 diabetes mellitus prior to insulin availability, exhibiting loss of subcutaneous fat and skeletal muscle. B, The same patient after insulin administration with restoration of subcutaneous fat depots and skeletal muscle. 29 Nonproliferative diabetic retinopathy impairs dark adaptation. A, A 57-year-old woman (hereinafter referred to as patient 73) with 21 years of type 2 diabetes mellitus, 20/25 visual acuity, and moderate nonproliferative diabetic retinopathy. The black circle represents the area of the retina that is assessed by the AdaptDx dark adaptometer. B, Dark adaptation curves of normal subjects (red circles) and patient 73 (blue squares) showing incomplete dark adaptation using AdaptDx dark adaptometer (Apeliotus Vision Sciences, Hershey, Pennsylvania), in spite of normal serum retinol, retinol binding protein, and retinyl ester levels. The dashed horizontal line is the 95% confidence interval for the upper limit of normal dark adaptation. Mild nonproliferative diabetic retinopathy impairs visual fields. A, A 56-year-old male with 9 years of type 2 diabetes mellitus, mild nonproliferative diabetic retinopathy, and 20/16 visual acuity. B, 24-2 Humphrey fields. C, Matrix freque Continue reading >>

Catabolic And Anabolic Faces Of Insulin Resistance And Their Disorders: A New Insight Into Circadian Control Of Metabolic Disorders Leading To Diabetes

Catabolic And Anabolic Faces Of Insulin Resistance And Their Disorders: A New Insight Into Circadian Control Of Metabolic Disorders Leading To Diabetes

Go to: Insulin resistance & circadian metabolism: comparison of reciprocal glucose-lipid regulation between lean, overfeeding, obesity & diabetes The survival of multicellular organisms depends on the organism's ability to maintain glucose homeostasis in times of low/high nutrient availability or low/high energy needs. These effects are achieved by the organism's ability to support equilibrium between energy-producing catabolic processes and energy-consuming anabolic pathways that make possible support of the metabolic homeostasis in fasting/feeding and sleep/wake cycles. Glucose metabolism is subject to fundamental systemic regulation that is controlled by the anabolic hormone insulin. In mammals, insulin is produced by pancreatic beta cells and released into the blood stream in response to increased concentrations of glucose. Insulin increases glucose uptake in the insulin-sensitive tissue (such as muscle and fat ones) and inhibits hepatic glucose production [5], thus serving as the primary regulator of blood glucose concentration in a narrow range between 4 and 7 mM in normal individuals [6]. Insulin increases the glucose uptake in cells by stimulating the translocation of the glucose transporter GLUT4 from intracellular sites to the cell surface. Insulin stimulates the glucose uptake primarily in muscles because up to 80% insulin-dependent glucose disposal occurs in activated skeletal muscles that require effective glucose delivery for its high-energy demand; whereas free fatty acids (FFA), especially saturated fatty acids (SFA) reduce the insulin-mediated glucose uptake in adipocytes and skeletal muscles [7]. Because of this, the increase in FFA induces IR that is contributing to supported glucose levels by its deficit. However, a similar IR response can occur at a Continue reading >>

Amino Acid And Protein Metabolism In Diabetes Mellitus.

Amino Acid And Protein Metabolism In Diabetes Mellitus.

Amino acid and protein metabolism in diabetes mellitus. Felig P , Wahren J , Sherwin R , Palaiologos G . In normal man, the fasting state is characterized by release of alanine and glutamine from muscle and in situ muscle catabolism of branched chain amino acids (lecucine, isoleucine, and valine). The alanine released by muscle is utilized by the liver for gluconeogenesis. Muscle nitrogen repletion occurs during protein feeding primarily by means of selective hepatic escape and muscle uptake of branched chain amino acids in ingested protein. In the diabetic, amino acid catabolism is exaggerated in the fasting state as reflected by increased uptake of alanine by the liver for gluconeogenesis and accelerated branched chain amino acid catabolism in muscle. After protein feeding, uptake of branched chain amino acids by muscle is reduced and these amino acids accumulate in increased amounts in arterial blood. Protein feeding also exaggerates the hyperglycemia of diabetes by causing an increase in hepatic glucose production. Diabetes is thus characterized by accelerated protein catabolism during fasting as well as diminished nitrogen repletion and hyperglycemia after protein feeding. The hyperketonemia of diabetes may however, have a restraining influence on protein catabolism thereby reducing alanine availability for gluconeogenesis. Continue reading >>

Glycemic Control In Diabetic Patients Undergoing Gynecologic Surgery

Glycemic Control In Diabetic Patients Undergoing Gynecologic Surgery

Glycemic Control in Diabetic Patients Undergoing Gynecologic Surgery Patients with diabetes undergoing surgery are at increased risk of morbidity and mortality from their hypermetabolic stress response, preoperative catabolic state, altered nutritional status, changes in circulation, immobility, and glucose and electrolyte derangements. As morbidity increases dramatically when preoperative blood glucose levels are elevated, all patients with diabetes should have an HgbA1C checked within three months of their intended procedure. Prior to surgery, care should be coordinated with the patients primary care provider or endocrinologist and an anesthesia consultation obtained to optimize glycemic control and other medical comorbidities. When possible, the patients diet and medications should be adjusted so they maintain a predominantly euglycemic state in the weeks before surgery. Fasting and postprandial blood glucoses should be checked as necessary to achieve euglycemia. The goal for the day of surgery is to avoid both hypoglycemia and excessive hyperglycemia. Patients with Type 1 diabetes may enter a ketoacidotic state even at low levels of hyperglycemia. Cancellation of surgery should be considered in non-emergent cases where blood glucoses are 400-500 mg/dL. No standardized, evidence-based algorithm for diabetes management exists for gynecologic surgery. Due to the risk of metabolic acidosis, metformin and other oral hypoglycemic agents should be withheld the day of surgery. On the morning of surgery, the patient should receive 50% of their usual NPH dose or 60-80% of their usual long-acting insulin analog (e.g. glargine or detemir) or pump basal insulin dose. Surgery induces a stress response with catecholamine and cortisol release, which reduces sensitivity to insulin. Continue reading >>

Protein Metabolism In Diabetes Mellitus

Protein Metabolism In Diabetes Mellitus

Volume 10, Issue 4 , October 1996, Pages 589-601 Author links open overlay panel Haitham S.Abu-Lebdeh K.SreekumaranNair Get rights and content Insulin deficiency is a protein catabolic state. In vivo studies have shown that insulin enhances short-side-chain amino acid intracellular uptake, stimulates transcription and translation of RNA, increases the gene expression of albumin and other proteins and inhibits liver protein breakdown enzymes. In IDDM patients most of the whole-body protein turnover studies have shown that insulin deficiency increases protein breakdown and increases amino acid oxidation and that these effects are reversed by insulin treatment. Recent studies have demonstrated that a substantial increase in leucine transamination during insulin deprivation contributes to leucine catabolism in IDDM patients. Protein synthesis in the insulin-deprived state is also increased although to a lesser extent than protein breakdown, and this increased whole-body protein synthesis is reduced with an insulin infusion; thus the effects of insulin are largely mediated through its effects on protein breakdown. The metabolic derangements in diabetes frequently involve disturbances in substrates and hormones other than insulin. The observed effects of insulin deficiency in diabetic patients vary in different body compartments; most of the effects of insulin on protein synthesis appear to occur in non-muscular tissues especially in the splanchnic area. In addition, insulin has a differential effect on hepatic protein synthesis, i.e. inhibits fibrinogen synthesis and promotes albumin synthesis. Insulin's anticatabolic effect in IDDM patients is largely due to its inhibition of protein breakdown. The net protein anabolism due to insulin occurs largely in skeletal muscle. In Continue reading >>

Effect Of A Catabolic State With Involuntary Weight Loss On Acute And Chronic Respiratory Disease

Effect Of A Catabolic State With Involuntary Weight Loss On Acute And Chronic Respiratory Disease

Effect of a Catabolic State With Involuntary Weight Loss on Acute and Chronic Respiratory Disease Authors: Authors: Robert H. Demling, MD, Leslie De Santi, RN This activity is intended for pulmonologists, critical care specialists, internists and pharmacists. The goal of this activity is to identify the clinical challenges that catabolism poses in respiratory disease; outline the pathophysiology of the disease in key conditions such as COPD and ARDS; and point out viable treatment options that clinicians can use to correct the condition. On completion of this continuing medical education offering, participants will be able to: Recognize the effect of decreasing lean body mass, especially muscle, during a catabolic insult on respiratory function. Identify the catabolic components of acute and chronic respiratory failure that cause protein-energy malnutrition and involuntary weight loss. Discuss ways to correct any existing malnutrition (PEM) or involuntary weight loss, to improve respiratory function through nutrition and anabolic strategies. Medical Education Collaborative, a nonprofit education organization, is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Medical Education Collaborative designates this educational activityfor a maximum of 1.5 category 1 credits toward the AMA Physician'sRecognition Award. Each physician should claim only those credits thathe/she actually spent in the activity. This CME activity is cosponsored by Medical EducationCollaborative and Medscape, also an ACCME-accredited provider. 1.8 contact hours of continuing education for RNs, LPNs, LVNs, and NPs.This activity is cosponsored with Medical Education Collaborative, Inc.(MEC) and Medscape. MEC is accr Continue reading >>

Protein And Energy Metabolism In Type 1 Diabetes

Protein And Energy Metabolism In Type 1 Diabetes

Protein and Energy Metabolism in Type 1 Diabetes We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Protein and Energy Metabolism in Type 1 Diabetes Profound metabolic changes occur in people with type 1 diabetes mellitus during insulin deprivation. These include an increase in basal energy expenditure and reduced mitochondrial function. In addition, protein metabolism is significantly affected during insulin deprivation. A greater increase in whole-body protein breakdown than protein synthesis occurs resulting in a net protein loss. During insulin deprivation the splanchnic bed has a net protein accretion which accounts for the total increase in whole-body protein synthesis while muscle is in a net catabolic state. Keywords: energy metabolism, insulin, mitochondria, protein synthesis, type 1 diabetes In the absence of insulin replacement type 1 diabetes is a catabolic condition with severe depletion of both energy stores and protein mass. Since most type 1 diabetic individuals are treated with insulin, a short period of insulin withdrawal in these individuals provides a model system to study the role of insulin in energy and protein metabolism. The causes of negative energy balance and protein catabolism have been extensively studied in people with type 1 diabetes and will be reviewed in this article. Profound changes in energy metabolism occur in people with type 1 diabetes mellitus (T1DM) during insulin deprivation in addition t Continue reading >>

Type 2 Diabetes Mellitus And The Catabolic Response To Surgery | Anesthesiology | Asa Publications

Type 2 Diabetes Mellitus And The Catabolic Response To Surgery | Anesthesiology | Asa Publications

Type 2 Diabetes Mellitus and the Catabolic Response to Surgery * Assistant Professor, Biochemist, # Resident, ** Professor, Department of Anesthesia, Assistant Professor, Nutrition and Food Science Center, Associate Professor, School of Dietetics and Human Nutrition, McGill University, Montreal, Canada. Assistant Professor, Department of Anesthesia and Intensive Care Medicine, Philipps-University Marburg, Germany. Clinical Science / Endocrine and Metabolic Systems Type 2 Diabetes Mellitus and the Catabolic Response to Surgery Anesthesiology 2 2005, Vol.102, 320-326. doi: Anesthesiology 2 2005, Vol.102, 320-326. doi: Thomas Schricker, Rejeanne Gougeon, Leopold Eberhart, Linda Wykes, Louise Mazza, George Carvalho, Franco Carli; Type 2 Diabetes Mellitus and the Catabolic Response to Surgery. Anesthesiology 2005;102(2):320-326. 2018 American Society of Anesthesiologists Type 2 Diabetes Mellitus and the Catabolic Response to Surgery You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account THE endocrine response to surgical tissue trauma is characterized by the activation of the hypothalamopituitary and sympathoadrenergic system, resulting in increased circulating concentrations of cortisol, glucagon, epinephrine, and norepinephrine. 1 All these hormones inhibit insulin secretion and/or counteract the peripheral action of insulin, leading to a state of impaired tissue insulin sensitivity. 2,3 Insulin resistance is thought to be one of the principal mechanisms responsible for the catabolic responses to surgery, including stimulated amino acid oxidation, muscle proteolysis, and gluconeogenesis along with decreased glucose utilization and hyperglycemia. 4,5 The similarity between th Continue reading >>

Protein Metabolism In Insulin-dependent Diabetes Mellitus.

Protein Metabolism In Insulin-dependent Diabetes Mellitus.

J Nutr. 1998 Feb;128(2 Suppl):323S-327S. doi: 10.1093/jn/128.2.323S. Protein metabolism in insulin-dependent diabetes mellitus. Endocrine Research Unit, Mayo Clinic and Foundation, Rochester, MN 55905, USA. Patients with insulin-dependent diabetes are in a catabolic state without insulin replacement. The mechanism of insulin's anticatabolic effect has been investigated in whole-body and regional tracer kinetic studies. Whole-body studies have demonstrated that there are increases in both protein breakdown and protein synthesis during insulin deprivation. Because the magnitude of the increase in protein breakdown is greater than the magnitude of the increase in protein synthesis, there is a net protein loss during insulin deprivation. Regional studies have shown that insulin replacement inhibits protein breakdown and synthesis in splanchnic tissue but only inhibits protein breakdown in skeletal muscle. Because the increase in protein synthesis in splanchnic tissues is greater than the increase in protein breakdown, insulin deprivation results in a net accretion of protein in the splanchnic bed. In contrast, in skeletal muscle, there is a net increase in protein breakdown during insulin deprivation, resulting in a net release of amino acids. There are no human data concerning the site of protein accretion in the splanchnic bed or the specific protein whose synthesis is increased during insulin deprivation. It appears that insulin exerts its overall anticatabolic effect in insulin-dependent diabetes mainly through the inhibition of muscle protein breakdown. Continue reading >>

Reduced Body Cell Mass In Type 2 Diabetes Mellitus: Reversal With A Diabetes-specific Nutritional Formula

Reduced Body Cell Mass In Type 2 Diabetes Mellitus: Reversal With A Diabetes-specific Nutritional Formula

Reduced body cell mass in type 2 diabetes mellitus: reversal with a diabetes-specific nutritional formula Authors: Tatti, Patrizio | di Mauro, Patrizia | Neri, Marisa | Pipicelli, Giuseppe | Strollo, Felice Affiliations: UOCA di Endocrinologia e Diabetologia, ASL RMH, via XXIV Maggio, Marino, 00047 Rome, Italy. e-mail: [email protected]; [email protected] | UOC Diabetologia e Dietologia, ASP Catanzaro, Catanzaro, Italy | UOC di Endocrinologia, INRCA, Rome, Italy Abstract: Subjects with type 2 diabetes are in a continuous catabolic state due to increased neoglycogensis during most of the fasting and the postprandial period. We compared the body cell mass index (BCMI) of 257 subjects with type 2 diabetes mellitus (T2DM) and 216 non-diabetic controls and found a statistically significant lower value in the diabetic subjects. This abnormality was reversed after 6 months of treatment with a diabetes-specific nutritional formula. Furthermore, in a population of 715 diabetic subjects without other diseases, we found that the BCMI was inversely correlated with the prevailing HbA1c and the duration of the disease. Keywords: T2DM, Nutrition, Body cell mass Journal: Mediterranean Journal of Nutrition and Metabolism , vol. 3, no. 2, pp. 133-136, 2010 Continue reading >>

Metabolic Pathways - Metabolism And Hormones - Diapedia, The Living Textbook Of Diabetes

Metabolic Pathways - Metabolism And Hormones - Diapedia, The Living Textbook Of Diabetes

There are three groups of molecules that form the core building blocks and fuel substrates in the body: carbohydrates (glucose and other sugars); proteins and their constituent amino acids; and lipids and their constituent fatty acids. The biochemical processes that allow these molecules to be synthesized and stored (anabolism) or broken down to generate energy (catabolism) are referred to as metabolic pathways. Glucose metabolism involves the anabolic pathways of gluconeogenesis and glycogenesis, and the catabolic pathways of glycogenolysis and glycolysis. Lipid metabolism involves the anabolic pathways of fatty acid synthesis and lipogenesis and the catabolic pathways of lipolysis and fatty acid oxidation. Protein metabolism involves the anabolic pathways of amino acid synthesis and protein synthesis and the catabolic pathways of proteolysis and amino acid oxidation. Under conditions when glucose levels inside the cell are low (such as fasting, sustained exercise, starvation or diabetes), lipid and protein catabolism includes the synthesis (ketogenesis) and utilization (ketolysis) of ketone bodies. The end products of glycolysis, fatty acid oxidation, amino acid oxidation and ketone body degradation can be oxidised to carbon dioxide and water via the sequential actions of the tricarboxylic acid cycle and oxidative phosphorylation, generating many molecules of the high energy substrate adenosine triphosphate (ATP). The interplay between glucose metabolism, lipid metabolism, ketone body metabolism and protein and amino acid metabolism is summarized in Figure 1. Amino acids can be a source of glucose synthesis as well as energy production and excess glucose that is not required for energy production can be stored as glycogen or metabolized to acetyl CoA and stored as fa Continue reading >>

Anabolism, Catabolism, & Insulin: The Definitions I Go By

Anabolism, Catabolism, & Insulin: The Definitions I Go By

I just want to provide some basic definitions to illustrate the terms that I’m using & how I understand them, & to try to state my basic understandings as clearly as I know how to. Anabolism: The phase of metabolism in which simple substances are synthesized into the complex materials of living tissue. Catabolism: The metabolic breakdown of complex molecules into simpler ones, often resulting in a release of energy. Both of my sources for these definitions (through the clickable links) are worth looking at, because they include dictionary definitions from several sources, as well as Wikipedia articles which explain in more depth. Basically, anabolism means taking simpler stuff & using it to build more complex stuff within the body: amino acids into protein into muscle, blood glucose into adipose tissue (body fat), etc. Catabolism does the opposite: it breaks larger, more complex molecules into simpler stuff, usually with a release of energy, for example, burning off fat through exercise or going on a low-calorie starvation diet that leads to the loss of lean muscle mass. Insulin is anabolic in these ways: Insulin tranfers blood glucose to the liver & to muscle cells to either be burned for energy, or to be synthesized (that is, built into) glycogen. Glycogen is “animal carbohydrate” which can be burnt (catabolized) when quick energy is needed for exercise or an emergency. Insulin is anabolic because it helps build glycogen. [Edit: I misstated that. Actually, glycogen itself isn’t burnt for energy. Rather, it’s converted back into glucose (a conversion stimulated by the catabolic hormone glucagon) & the resulting glucose can then be burnt for energy.] Insulin transfers excess blood glucose, that is more than the body needs for its immediate energy requirements Continue reading >>

Insulin Treatment Reverses The Increase In Atrogin-1 Expression In Atrophied Skeletal Muscles Of Diabetic Rats With Acute Joint Inflammation

Insulin Treatment Reverses The Increase In Atrogin-1 Expression In Atrophied Skeletal Muscles Of Diabetic Rats With Acute Joint Inflammation

Editor who approved publication: Professor Garry Walsh Clara Maria Pinheiro-Dardis,1 Vnia Ortega Gutierres,1 Renata Pires Assis,1 Sabrina Messa Peviani,2 Gabriel Borges Delfino,2 Joo Luiz Quagliotti Durigan,3 Tania de Ftima Salvini,2 Amanda Martins Baviera,1 Iguatemy Loureno Brunetti1 1So Paulo State University (UNESP), School of Pharmaceutical Sciences, Department of Clinical Analysis, Araraquara, So Paulo, Brazil; 2Federal University of So Carlos (UFSCar), Department of Physical Therapy, So Carlos, So Paulo, Brazil; 3Physical Therapy Division, University of Brasilia, Brasilia, Federal District, Brazil Background: The aim of this study was to evaluate the changes in biomarkers of skeletal muscle proteolysis (atrogin-1, muscle RING finger-1 protein [MuRF-1]) and inflammation (nuclear factor kappa-B) in skeletal muscles of rats under two catabolic conditions, diabetes mellitus (DM) and acute joint inflammation, and the effects of insulin therapy. Materials and methods: Male Wistar rats were divided into groups without diabetes normal (N), saline (NS), or -carrageenan (NCa) injection into the tibiotarsal joint and groups with diabetes diabetes (D), plus insulin (DI), saline (DS), or -carrageenan (DCa) injection into the tibiotarsal joint, or -carrageenan injection and treatment with insulin (DCaI). Three days after -carrageenan injection (17 days after diabetes induction), tibialis anterior (TA) and soleus (SO) skeletal muscles were used for analysis. Results: DM alone caused a significant decrease in the mass of TA and SO muscles, even with low levels of atrogenes (atrogin-1, MuRF-1), which could be interpreted as an adaptive mechanism to spare muscle proteins under this catabolic condition. The loss of muscle mass was exacerbated when -carrageenan was administered in t Continue reading >>

Protein Metabolism In Insulin-dependent Diabetes Mellitus

Protein Metabolism In Insulin-dependent Diabetes Mellitus

Protein Metabolism in Insulin-Dependent Diabetes Mellitus Endocrine Research Unit, Mayo Clinic and Foundation, Rochester, MN To whom correspondence should be addressed: Mayo Clinic and Foundation, Eisenberg 3-G, 200 First Street S. W., Rochester, MN 55905. Search for other works by this author on: Endocrine Research Unit, Mayo Clinic and Foundation, Rochester, MN Search for other works by this author on: The Journal of Nutrition, Volume 128, Issue 2, 1 February 1998, Pages 323S327S, Michael Charlton, K. Sreekumaran Nair; Protein Metabolism in Insulin-Dependent Diabetes Mellitus, The Journal of Nutrition, Volume 128, Issue 2, 1 February 1998, Pages 323S327S, Patients with insulin-dependent diabetes are in a catabolic state without insulin replacement. The mechanism of insulin's anticatabolic effect has been investigated in whole-body and regional tracer kinetic studies. Whole-body studies have demonstrated that there are increases in both protein breakdown and protein synthesis during insulin deprivation. Because the magnitude of the increase in protein breakdown is greater than the magnitude of the increase in protein synthesis, there is a net protein loss during insulin deprivation. Regional studies have shown that insulin replacement inhibits protein breakdown and synthesis in splanchnic tissue but only inhibits protein breakdown in skeletal muscle. Because the increase in protein synthesis in splanchnic tissues is greater than the increase in protein breakdown, insulin deprivation results in a net accretion of protein in the splanchnic bed. In contrast, in skeletal muscle, there is a net increase in protein breakdown during insulin deprivation, resulting in a net release of amino acids. There are no human data concerning the site of protein accretion in the splanchn Continue reading >>

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