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Type 2 Diabetes Molecular Level

68: Insulin Action, Insulin Resistance, And Type 2 Diabetes Mellitus

68: Insulin Action, Insulin Resistance, And Type 2 Diabetes Mellitus

Abstract Abstract Diabetes mellitus is a syndrome characterized by elevated levels of glucose in the plasma. The American Diabetes Association has recently proposed revised criteria for the diagnosis of diabetes: (a) a fasting plasma glucose level >126 mg/dl, or (b) a plasma glucose level >200 mg/dl at 2 h after the ingestion of oral glucose (75 g), or (c) random plasma glucose >200 mg/dl. Diabetes is a heterogeneous clinical syndrome with multiple etiologies. Type 1 diabetes is caused by destruction of pancreatic beta cells, most often by autoimmune mechanisms. Type 2 diabetes (the most common form of diabetes, accounting for >90 percent of patients) is caused by a combination of two physiological defects: resistance to the action of insulin combined with a deficiency in insulin secretion. Although the molecular basis of the common form of type 2 diabetes has not been elucidated, it is thought to result from genetic defects that cause both insulin resistance and insulin deficiency. Type 2 diabetes generally has onset after the age of 40. Unlike type 1 diabetes, type 2 diabetes is usually associated with relatively mild hyperglycemia, and ketoacidosis seldom develops. Gestational diabetes mellitus is a form of diabetes that has its initial onset during pregnancy, and resolves after the end of the pregnancy. Insulin exerts multiple effects upon target cells—especially skeletal muscle, liver, and adipose tissue. In general, insulin promotes storage of fuels (e.g., glycogen and triglyceride), and inhibits the breakdown of stored fuel. To accomplish these general physiological functions, insulin exerts multiple specific actions upon target cells. For example, insulin promotes recruitment of glucose transporters from intracellular vesicles to the plasma membrane, thereby s Continue reading >>

Insulin Resistance

Insulin Resistance

Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults.[1] Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose.[2] In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose. People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome. Insuli Continue reading >>

Pathophysiology And Pathogenesis Of Type 2 Diabetes

Pathophysiology And Pathogenesis Of Type 2 Diabetes

Type 2 Diabetes Overview Type 2 Diabetes at the Cellular Level Pathophysiology of Type 2 Diabetes Insulin Resistance The Impact of Cortisol Cellular Inflammation Advanced Glycation End Products (AGEs) The 7 Stages of Type 2 Diabetes Pathogenesis Red Blood Cell Lifecycle Why Understanding Diabetes Is So Important Next Steps to Reverse Your Diabetes Clinical References Author Sidebar: When I was in the hospital (and after I came out of the coma), I remember the doctors and nurses telling me that I had Type 2 diabetes. They said I had a very severe blood sugar problem because my blood sugar was over 1300. And, because my blood sugar was so high, I was given insulin to bring my blood sugar back down. At the time, this all made sense to me. So, I concluded (at that time) that once my blood sugar returned to normal, everything would be okay. But, instead, I was told that once my blood sugar returned to normal, everything would not be okay because I would still be diabetic. Needless to say, this was confusing and disheartening. But, I quickly realized that "high blood sugar" was not the real problem! -- it was a symptom of the problem. And, the real problem of having Type 2 diabetes was more than just a blood sugar problem. Type 2 diabetes is the most common form of diabetes, with more than 90% of diabetics being Type 2; and, 5% to 10% being Type 1. Type 2 diabetes mellitus is a heterogeneous disorder with varying prevalence among different ethnic groups. In the United States the populations most affected are Native Americans, particularly in the desert Southwest, Hispanic-Americans, African-Americans, and Asian-Americans. However, Caucasian-Americans are also affected, but not at the same disproportionate percentage levels. Type 2 Diabetes Impacts ALL groups and cultures! The Continue reading >>

Molecular Mechanism Of Insulin Resistance In Obesity And Type 2 Diabetes

Molecular Mechanism Of Insulin Resistance In Obesity And Type 2 Diabetes

Molecular Mechanism of Insulin Resistance in Obesity and Type 2 Diabetes Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA. Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA. Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA. Correspondence to Young-Bum Kim, Ph.D. Beth Israel Deaconess Medical Center, 330 Brookline Ave., Center for Life Science-736, Boston, MA 02115, USA. Tel: 1-617-735-3216, Fax: 1-617-735-3323, [email protected] Copyright 2010 The Korean Association of Internal Medicine This article has been cited by other articles in PMC. Insulin resistance is a major risk factor for developing type 2 diabetes caused by the inability of insulin-target tissues to respond properly to insulin, and contributes to the morbidity of obesity. Insulin action involves a series of signaling cascades initiated by insulin binding to its receptor, eliciting receptor autophosphorylation and activation of the receptor tyrosine kinase, resulting in tyrosine phosphorylation of insulin receptor substrates (IRSs). Phosphorylation of IRSs leads to activation of phosphatidylinositol 3-kinase (PI3K) and, subsequently, to activation of Akt and its downstream mediator AS160, all of which are important steps for stimulating glucose transport induced by insulin. Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired insulin-dependent PI3K activation and downstream signaling. This review focuses on the molecular basis of skeletal muscle insulin resist Continue reading >>

Diabetes Mellitus At A Molecular Level

Diabetes Mellitus At A Molecular Level

We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime. This presentation is all about the well-known disease "Diabetes". I have tried to focus on the molecular level of the disease, and I've discussed in detail the proteins and genes related in the process. I definitely looked through many references, watched many videos and read many articles about it. I was pretty much confused, but thanks to God, I was finally able to put together all I had learned into a nice, neat PowerPoint presentation. Wether you are a college student seeking a presentation about diabetes, or maybe just a normal person wanting to get some info, maybe a patient with diabetes, then you should be in the right place. My presentation should help you get through! I have first begun with an introduction to the disease, including some data from International Diabetes Federation to show the huge number of people worldwide having diabetes. I have then talked about how our body functions normally without diabetes. This will help you understand what goes wrong during the disease. After that, I have discussed both type 1 and type 2 diabetes and what causes each type at a molecular level as well as talking about some differences. Then I've come to talk about symptoms and complications of diabetes. The signs that could indicate someone has diabetes, and if someone has it for a long time, it's going to have impact on the various body systems and cause other diseases - known as complications. So I have also made clear what the complications of diabetes are in very easy to understand diagrams. Finally, I have talked about how diabetes may be diagnosed and what the possible treatments are for each type. I've used many graphi Continue reading >>

Molecular Mechanisms Of Skeletal Muscle Insulin Resistance In Type 2 Diabetes

Molecular Mechanisms Of Skeletal Muscle Insulin Resistance In Type 2 Diabetes

Molecular Mechanisms of Skeletal Muscle Insulin Resistance in Type 2 Diabetes Author(s): Karim Bouzakri , Heikki A. Koistinen , Juleen R. Zierath . Department of Surgical Sciences, Section for Integrative Physiology, Karolinska Institutet vonEulers vag 4A, 4th floor, SE-171 77 Stockholm, Sweden. Type 2 (non-insulin-dependent) diabetes mellitus afflicts millions of people worldwide and is one of the main causes of morbidity and mortality. Current therapeutic agents to treat Type 2 diabetes are insufficient and thus, newer approaches are desperately needed. Type 2 diabetes is manifested by progressive metabolic impairments in tissues such as skeletal muscle, adipose tissue and liver, such that these tissues become less responsive to insulin. Skeletal muscle is quantitatively the most important tissue involved in maintaining glucose homeostasis under insulin-stimulated conditions, and is a major site of insulin resistance in Type 2 diabetic patients. At the cellular level, glucose transport into skeletal muscle is the rate-limiting step for whole body glucose uptake and a primary site of insulin resistance in Type 2 diabetes. Thus, skeletal muscle is a key insulin target tissue that harbours intrinsic defects that impinges upon whole body glucose homeostasis. Here, we review the current knowledge of signalling events that regulate glucose transport in human skeletal muscle. Keywords: adipose tissue, glucose transport, insulin resistance, insulin signalling, obesity, skeletal muscle, type (non-insulin dependent) diabetes mellitus Title: Molecular Mechanisms of Skeletal Muscle Insulin Resistance in Type 2 Diabetes Author(s):Karim Bouzakri, Heikki A. Koistinen and Juleen R. Zierath Affiliation:Department of Surgical Sciences, Section for Integrative Physiology, Karolinska In Continue reading >>

Type 2 Diabetes Mellitus (t2dm): Biological Overview From Pathways To Organelles And Its Translation Toward A Torpid Wound Healing Process

Type 2 Diabetes Mellitus (t2dm): Biological Overview From Pathways To Organelles And Its Translation Toward A Torpid Wound Healing Process

Received date: July 16, 2013; Accepted date: August 14, 2013; Published date: August 20, 2013 Citation: Berlanga-Acosta J, Lpez-Saura P, Guillen-Prez I, Guillen-Nieto G, Acevedo-Castro B, et al. (2013) Type 2 Diabetes Mellitus (T2DM): Biological Overview from Pathways to Organelles and its Translation toward a Torpid Wound Healing Process. J Diabetes Metab 4:285. doi: 10.4172/2155-6156.1000285 Copyright: 2013 Berlanga-Acosta J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. T2DM is a heterogeneous group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Hyperglycemia may simply represent the tip of a broad series of molecular events from mitochondrial damages, to epigenetic and metabolic pathways deregulations. At the same time, hyperglycemia appears as the most proximal trigger for the onset and perpetual progression of multi-organ complications even under normoglycemic conditions. Thus, the initial hyperglycemic hit translates into a permanently harmful cellular imprinting as has been demonstrated in diabetic donors cells after several passages and cultured in ideal conditions. The wound healing failure along with the inability of the innate immunity to control peripheral infections is the hybrid that determines that 85% of all non-traumatic lower extremity amputations are practiced in diabetic subjects. Diabetic wounds exhibit a complex networking of inflammatory cytokines, local proteases, cytotoxic reactive oxygen and nitrogen species and a polymicrobial biofilm that impose a stagnant phenotype. All t Continue reading >>

Pathogenesis Of Type 2 Diabetes Mellitus

Pathogenesis Of Type 2 Diabetes Mellitus

INTRODUCTION Type 2 diabetes mellitus is characterized by hyperglycemia, insulin resistance, and relative impairment in insulin secretion. It is a common disorder with a prevalence that rises markedly with increasing degrees of obesity (figure 1) [1]. The prevalence of type 2 diabetes has risen alarmingly in the past decade [2], in large part linked to the trends in obesity and sedentary lifestyle [3]. PATHOPHYSIOLOGY Understanding the pathogenesis of type 2 diabetes is complicated by several factors [4]. Patients present with a combination of varying degrees of insulin resistance and relative insulin deficiency, and it is likely that both contribute to type 2 diabetes [5-7]. Furthermore, each of the clinical features can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. Moreover, hyperglycemia itself can impair pancreatic beta-cell function and exacerbate insulin resistance, leading to a vicious cycle of hyperglycemia causing a worsening metabolic state [8]. Type 2 diabetes is often accompanied by other conditions, including hypertension, high serum low-density lipoprotein (LDL) cholesterol concentrations, and low serum high-density lipoprotein (HDL) cholesterol concentrations that, like type 2 diabetes, increase cardiovascular risk. This constellation of clinical conditions is referred to as the metabolic syndrome [9]. Hyperinsulinemia occurring in response to insulin resistance may play an important role in the genesis of these abnormalities. Increased free fatty acid levels, inflammatory cytokines from fat, and oxidative factors have all been implicated in the pathogenesis of metabolic syndrome, type 2 diabetes, and their cardiovascular complications. (See "The metabolic syndrome (insulin re Continue reading >>

Diabetes: Mechanism, Pathophysiology And Management-a Review

Diabetes: Mechanism, Pathophysiology And Management-a Review

Anees A Siddiqui1*, Shadab A Siddiqui2, Suhail Ahmad, Seemi Siddiqui3, Iftikhar Ahsan1, Kapendra Sahu1 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi (INDIA)-110062. School of Pharmacy, KIET, Ghaziabad U.P. SGC college of Pharmacy, Baghpat(UP) Corresponding Author:Anees A Siddiqui E-mail: [email protected] Received: 20 February 2011 Accepted: 02 May 2011 Citation: Anees A Siddiqui, Shadab A Siddiqui, Suhail Ahmad, Seemi Siddiqui, Iftikhar Ahsan, Kapendra Sahu “Diabetes: Mechanism, Pathophysiology and Management-A Review” Int. J. Drug Dev. & Res., April-June 2013, 5(2): 1-23. Copyright: © 2013 IJDDR, Anees A Siddiqui et al. This is an open access paper distributed under the copyright agreement with Serials Publication, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Related article at Pubmed, Scholar Google Visit for more related articles at International Journal of Drug Development and Research The prevalence of diabetes is rapidly rising all over the globe at an alarming rate. Over the last three decades, the status of diabetes has been changed, earlier it was considered as a mild disorder of the elderly people. Now it becomes a major cause of morbidity and mortality affecting the youth and middle aged people. According to the Diabetes Atlas 2006 published by the International Diabetes Federation, the number of people with diabetes in India currently around 40.9 million is expected to rise to 69.9 million by 2025 unless urgent preventive steps are taken. The main force of the epidemic of diabetes is the rapid epidemiological transition associated with changes in dietary patterns and decreased physical activity a Continue reading >>

Insulin Signaling In Type 2 Diabetes

Insulin Signaling In Type 2 Diabetes

Abstract Type 2 diabetes originates in an expanding adipose tissue that for unknown reasons becomes insulin resistant. Insulin resistance reflects impairments in insulin signaling, but mechanisms involved are unclear because current research is fragmented. We report a systems level mechanistic understanding of insulin resistance, using systems wide and internally consistent data from human adipocytes. Based on quantitative steady-state and dynamic time course data on signaling intermediaries, normally and in diabetes, we developed a dynamic mathematical model of insulin signaling. The model structure and parameters are identical in the normal and diabetic states of the model, except for three parameters that change in diabetes: (i) reduced concentration of insulin receptor, (ii) reduced concentration of insulin-regulated glucose transporter GLUT4, and (iii) changed feedback from mammalian target of rapamycin in complex with raptor (mTORC1). Modeling reveals that at the core of insulin resistance in human adipocytes is attenuation of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sensitivity and signal strength throughout the signaling network. Model simulations with inhibition of mTORC1 are comparable with experimental data on inhibition of mTORC1 using rapamycin in human adipocytes. We demonstrate the potential of the model for identification of drug targets, e.g. increasing the feedback restores insulin signaling, both at the cellular level and, using a multilevel model, at the whole body level. Our findings suggest that insulin resistance in an expanded adipose tissue results from cell growth restriction to prevent cell necrosis. Continue reading >>

Biology Diagrams: Type 2 Diabetes At The Cellular Level

Biology Diagrams: Type 2 Diabetes At The Cellular Level

Author's Perspective: I loved biology when I was in school. But, now I really loved biology because it gave me a better insight into understanding diabetes pathology and how to defeat the disease at the cellular level. It also helped me to break down the complex medical terms and describe the biology in layman's terms. Being able to explain the biology of diabetes at the cell level in layman's terms provided the audience with a clear understanding of the biochemical and hormonal processes that fuel Type 2 diabetes. The benefit of this insight (to you) will empower you because you will have enough of an understanding of diabetes to comprehend whether the diabetes book that you are planning to purchase will actually help you. You will also have enough of an understanding to ask your doctor the right questions and give you some insight into what your doctor really knows about diabetes. This is not meant for you to go behind your doctor's back, but, to understand his/her limitations so that you don't get angry or frustrated with his recommendations for your diabetes. In addition, this information provides insight into how diabetes is damaging your body. This information will help you better understand the changes you need to make in order to control your diabetes and achieve tighter blood glucose control, insulin utilization, and blood glucose stability. By understanding these biological processes, you will gain a better insight into how to successfully reverse and defeat your diabetes. As a bonus, especially for healthcare professionals, you will gain an insight into how the author used "reverse engineering" as one of his engineering methodologies to better define how to control the disease, stop the progression of the disease, and then reverse the progression of Type 2 di Continue reading >>

What Is Type 2 Diabetes?

What Is Type 2 Diabetes?

Type 2 diabetes is the most common form of diabetes. You have Type 2 diabetes if your tissues are resistant to insulin, and if you lack enough insulin to overcome this resistance. You have Type 2 diabetes if your tissues are resistant to insulin, and if you lack enough insulin to overcome this resistance. Type 2 diabetes is the most common form of diabetes of diabetes worldwide and accounts for 90-95% of cases. Risk Factors Your risk of type 2 diabetes typically increases when you are: Other risk factors are: Family history of diabetes in close relatives Being of African, Asian, Native American, Latino, or Pacific Islander ancestry High blood pressure High blood levels of fats, known as triglycerides, coupled with low levels of high-density lipoprotein, known as HDL, in the blood stream Prior diagnosis of pre-diabetes such as glucose intolerance or elevated blood sugar In women, a history of giving birth to large babies (over 9 lbs) and/or diabetes during pregnancy Type 2 diabetes is strongly inherited These are some of the statistics: 80-90% of people with Type 2 diabetes have other family members with diabetes. 10-15% of children of a diabetic parent will develop diabetes. If one identical twin has type 2 diabetes, there is up to a 75% chance that the other will also be diabetic. There are many genetic or molecular causes of type 2 diabetes, all of which result in a high blood sugar. As yet, there is no single genetic test to determine who is at risk for type 2 diabetes. To develop type 2 diabetes, you must be born with the genetic traits for diabetes. Because there is a wide range of genetic causes, there is also a wide range in how you will respond to treatment. You may be easily treated with just a change in diet or you may need multiple types of medication. The ha Continue reading >>

Molecular Mechanisms Of Insulin Resistance In Type 2 Diabetes Mellitus

Molecular Mechanisms Of Insulin Resistance In Type 2 Diabetes Mellitus

Molecular mechanisms of insulin resistance in type 2 diabetes mellitus Vandana Saini, Department of Biochemistry, Lady Hardinge Medical College, New Delhi 110001, India. Author contributions: Saini V contributed solely to this work. Correspondence to: Vandana Saini, MD, Department of Biochemistry, Lady Hardinge Medical College, New Delhi 110001, India. [email protected] Received 2010 Jan 18; Revised 2010 Jun 22; Accepted 2010 Jun 29. Copyright 2010 Baishideng Publishing Group Co., Limited. All rights reserved. This article has been cited by other articles in PMC. Free fatty acids are known to play a key role in promoting loss of insulin sensitivity in type 2 diabetes mellitus but the underlying mechanism is still unclear. It has been postulated that an increase in the intracellular concentration of fatty acid metabolites activates a serine kinase cascade, which leads to defects in insulin signaling downstream to the insulin receptor. In addition, the complex network of adipokines released from adipose tissue modulates the response of tissues to insulin. Among the many molecules involved in the intracellular processing of the signal provided by insulin, the insulin receptor substrate-2, the protein kinase B and the forkhead transcription factor Foxo 1a are of particular interest, as recent data has provided strong evidence that dysfunction of these proteins results in insulin resistance in vivo. Recently, studies have revealed that phosphoinositidedependent kinase 1-independent phosphorylation of protein kinase C causes a reduction in insulin receptor gene expression. Additionally, it has been suggested that mitochondrial dysfunction triggers activation of several serine kinases, and weakens insulin signal transduction. Thus, in this review, the current developmen Continue reading >>

Exercise And Type 2 Diabetes: Molecular Mechanisms Regulating Glucose Uptake In Skeletal Muscle

Exercise And Type 2 Diabetes: Molecular Mechanisms Regulating Glucose Uptake In Skeletal Muscle

Exercise and type 2 diabetes: molecular mechanisms regulating glucose uptake in skeletal muscle Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts Address for reprint requests and other correspondence: K. I. Stanford, Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Dept. of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215 (e-mail: [email protected] ). Received 2014 Jul 2; Accepted 2014 Oct 2. Copyright 2014 The American Physiological Society This article has been cited by other articles in PMC. Exercise is a well-established tool to prevent and combat type 2 diabetes. Exercise improves whole body metabolic health in people with type 2 diabetes, and adaptations to skeletal muscle are essential for this improvement. An acute bout of exercise increases skeletal muscle glucose uptake, while chronic exercise training improves mitochondrial function, increases mitochondrial biogenesis, and increases the expression of glucose transporter proteins and numerous metabolic genes. This review focuses on the molecular mechanisms that mediate the effects of exercise to increase glucose uptake in skeletal muscle. diabetes is a complex disease that affects millions of people worldwide. There are 23.6 million people in the United States or 8% of the population that have diabetes, a number that has doubled over the last 15 yr and is continuing to increase at epidemic rates ( 56 ). It is predicted that 1 in 3 adults in the United States will have diabetes by 2050, yielding enormous tolls at individual, public health, and economic levels ( 56 ). Type 2 diabetes arises from a combination of gen Continue reading >>

Review Alterations Of Insulin Signaling In Type 2 Diabetes: A Review Of The Current Evidence From Humans

Review Alterations Of Insulin Signaling In Type 2 Diabetes: A Review Of The Current Evidence From Humans

Abstract A generally accepted view posits that insulin resistant condition in type 2 diabetes is caused by defects at one or several levels of the insulin-signaling cascade in skeletal muscles, adipose tissue and liver, that quantitatively constitute the bulk of the insulin-responsive tissues. Hence, the gradual uncovering of the biochemical events defining the intracellular signaling of insulin has been quickly followed by clinical studies on humans attempting to define the molecular defect(s) responsible for the establishment of the insulin resistant state. While the existence of molecular defects within the insulin signal transduction machinery is undisputed, contrasting data exist on what is the principal molecular alteration leading to insulin resistance. Such discrepancies in the literature may depend on: 1) different subject characteristics, 2) methodological differences 3) small cohorts of subjects, and – not least – 4) intrinsic limitations in studying every detail of the insulin signaling cascade. Here, we review the studies on humans exploring the defects of the insulin signaling cascade generated by insulin resistance and type 2 diabetes, focusing on muscle and adipose tissue – which account for most of the glucose disposal capacity of the body – with focus on the unresolved discrepancies present in the literature. Abbreviations aPKCs atypical protein kinases C GS glycogen synthase GSK-3 glycogen synthase kinase-3 IR insulin receptor JNK Jun N-terminal kinase MAPK Mitogen-activated protein kinase mTOR mammalian target of rapamycin PDK1 phosphoinositide-dependent protein kinase 1 PH domain pleckstrin homology domain PTB domain phosphotyrosine binding domain PI3K phosphoinositide 3-kinase PIP3 phosphatidylinositol (3,4,5) trisphosphate PKB protein kina Continue reading >>

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