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The brain is crucial for the regulation of whole-body metabolism and behavior. The pancreas-derived hormone insulin modulates brain function and affects energy metabolism as well as cognition. This is partially achieved by modulating several types of brain cell populations including those relevant to satiety and reward. Importantly, brains of Alzheimer´s disease patients exhibit a signature of brain insulin resistance with perturbed brain metabolism. This book will cover the basics of insulin signaling in the brain and will describe concepts of insulin resistance, a feature of type 2 diabetes. Moreover insulin´s effect on cognitive function will be pointed out and the association between brain insulin resistance and neurodegenerative diseases discussed. Additionally, potential behavioral and pharmacological concepts which can affect brain insulin signaling will be summarized.Key Features: Summarizes insulin and the closely related IGF-1 receptor signaling Depicts concepts of insulin resistance Highlights the importance of conserved brain insulin signaling for brain function, metabolism, and behavior Describes potential behavioral and pharmacological approaches to support brain insulin signaling

Insulin: Deficiency, Excess and Resistance in Human Disease provides an overview of the role of insulin in the pathogenesis of prevalent non-communicable diseases such as obesity, type 2 diabetes, cardiovascular disease, and cancer, along with a comprehensive review of insulin replacement therapies and novel cardioprotective and insulin-sensitizing drugs. Notable advances in precision diagnosis and therapy for single gene subtypes of diabetes in recent years are also discussed.The discovery of insulin and its lifesaving introduction into clinical practice is one of the most celebrated accomplishments of medical science. However, despite decades of progress and major technical advances, the goal of providing insulin replacement therapy that truly mimics normal physiology remains elusive. - Presents etiology and pathogenesis of insulin deficiency, insulin excess and insulin resistance in a wide spectrum of human diseases, ranging from rare to highly prevalent disorders - Discusses the latest developments in the diagnosis and management of insulin-related disorders and prospects for future developments - Explores the increasingly complex pharmacological landscape that comprises a bewildering range of drug-based interventions

Over the last decades, the growing prevalence of insulin resistance has dramatically contributed to the global epidemic of metabolic syndrome, obesity, type 2 diabetes mellitus, and cardiovascular disease. Therefore, there is an unmet need for novel nutritional and pharmacological strategies aimed to prevent or treat insulin resistance and its related comorbidities. This book presents a comprehensive overview of the pathophysiology and clinical consequences of insulin resistance in different settings, describing novel diagnostic biomarkers and molecular targets of this condition.

This volume, written by renowned experts, provides complete coverage of the main genetic conditions associated with diabetes. Divided into five sections, it offers insights into genetic defects involving the pancreatic beta cell, extreme insulin resistance, ciliopathies, obesity and glucose metabolism, chromosomal defects, and other genetic conditions associated with increased susceptibility to diabetes. Other topics include the various subtypes of monogenic diabetes, such as the neonatal form and the Wolfram syndrome, as well as chromosomal defects leading to complex conditions affiliated with diabetes, like Trisomy 21 or Prader-Willi syndrome. There are also chapters dedicated to the poorly explored relationships between metabolism and neurodegenerative disorders like Friedreich's ataxia and muscular dystrophy. This book is a reference for every pediatric and adult endocrinologist and diabetologist, even experienced ones, with an interest in the intricacies and protean aspects of disorders of glucose metabolism secondary to genetic diseases.

Summary of The Obesity Code by Jason Fung | Includes Analysis Preview: The Obesity Code addresses the history, causes, and treatments of obesity and today's rising obesity rates. By understanding it through scientific and social study, obesity becomes less of a blanket term for metabolic complications and a more tangible problem with real, though not widely practiced, solutions. The main problem with treating obesity is that many doctors and their obese patients don't know what actually causes obesity. Often, health experts believe that weight gain results from consuming too many calories while not expending enough calories, a theory known as “calories in, calories out.” However, decades of research has proven that this obesity model is problematic and oversimplified. Calorie consumption and expenditure are not independent of each other. If people decrease calorie consumption in an effort to lose weight, their body compensates by slowing down processes such as metabolism to expend fewer calories. Also, exercise is not nearly as instrumental in weight loss as was once thought… PLEASE NOTE: This is key takeaways and analysis of the book and NOT the original book. Inside this Instaread Summary of The Obesity Code · Overview of the Book · Important People · Key Takeaways · Analysis of Key Takeaways About the Author With Instaread, you can get the key takeaways, summary and analysis of a book in 15 minutes. We read every chapter, identify the key takeaways and analyze them for your convenience.

FROM NEW YORK TIMES BESTSELLING AUTHOR DR. JASON FUNG: The landmark book that is helping thousands of people lose weight for good. Harness the power of intermittent fasting for lasting weight loss. Understand the science of weight gain and insulin resistance. Stop suffering and ditch calorie counting, yoyo diets, and excessive exercise. In this highly readable book, Dr. Jason Fung, long considered the founder of intermittent fasting, sets out an original theory of obesity and weight gain. He reveals that everything you've been told about how to lose weight is wrong: weight gain is driven by hormones, and only by understanding the effects of insulin and insulin resistance can we achieve lasting weight loss. Dr. Fung shares five basic steps to controlling your insulin for better health. And he explains how to use intermittent fasting to break the cycle of insulin resistance and reach a healthy weight—permanently.

Type 2 diabetes mellitus is associated with a greater risk of developing atherosclerotic macrovascular diseases like myocardial infarction, stroke, and peripheral vascular disease. There is 2- to 4-fold increased risk of atherosclerotic heart disease and stroke in diabetic patients compared to non-diabetic patients. As the prevalence of type 2 diabetes is increasing rapidly, this diabetes related atherosclerotic disease is predicted to be a major public health problem. Atherosclerosis is a complex process and in diabetic patients, it behaves differently with increased lesion progression and severity. This accelerated atherosclerotic process in diabetics is explained on the basis of several risk factors like hyperglycemia, dyslipidemia, accelerated formation of advanced glycation end products, increased oxidative stress, and genetic factors. It is difficult to establish precisely the elements responsible for this atherosclerosis in diabetics, but by epidemiological, clinical, and by animal studies, it has been possible to get an idea of this problem in diabetics. Of the several risk factors for atherosclerosis in diabetes, dyslipidemia is the leading one, and an insight into the pathophysiologic relation of isolated triglyceridemia in Indian diabetics with the identification of the targets for control of lipids in diabetes (practical vs. ideal) needs to be well understood by the treating physician. This book is designed to address such issues with supportive typical clinical scenarios, with which the readers will be able to identify. Thus, it provides an excellent opportunity to widen one's perspective in this area.

The insulin resistance syndrome can be defined as insulin resistance, compensatory hyperinsulinemia, and their associated co-morbidities. Clinically, the term insulin resistance syndrome describes a constellation of abnormalities such as obesity, hypertension, dyslipidemia, type 2 diabetes/hyperglycemia, and coronary artery disease. Insulin is responsible for glucose uptake into the body cells and tissues. The response of the cells to insulin varies from individual to individual. In some individuals, the tissue response to insulin may be diminished. This means that even with adequate levels of insulin, the glucose uptake into the cells and tissues is not optimal. This results in a compensatory over-secretion of insulin from the pancreas. The persistence of high levels of insulin in the blood or hyperinsulinemia is thought to be responsible for some of the abnormalities associated with this condition. However, the exact causal association of the condition with these disorders and the pathophysiology of their evolution are unclear. The most common underlying mechanism proposed is increased free fatty acids from abdominal fat in individuals with central obesity. This leads to deranged insulin signaling, reduced muscular glucose uptake, increased triglyceride synthesis, and hepatic gluconeogenesis. A genetic basis of the disease as well as several other factors such as tumor necrosis factor-a, adiponectin, leptin, Interleukin-6, and some adipokines have also been implicated. Insulin resistance syndrome is of clinical significance because of its association with potentially debilitating conditions that contribute to long-term morbidity and even mortality of the individual. People with insulin resistance syndrome are at an increased risk of developing type 2 diabetes, hypertension, dyslipidemia, myocardial infarction, polycystic ovarian disease, and fatty liver. In this book, we have tried to collate the experiences of the pioneers of this field on the subject and provide the reader a comprehensive view on the topic along with practical management points, which we are sure will benefit the physicians in their clinical practice. The contributors have focused on the condition as is prevalent in our subcontinent and have tried to give an insight on the issues pertaining to the same with a topical flavor.

Cardiometabolic disease is the leading cause of death in many parts of the world. There are many potentially modifiable and non-modifiable risk factors associated with the same. Although with the recent advances in management and preventive strategies the mortality rates have reduced, but no patient actually achieves an adequate control of the CVD risk factors with the declining quality of life. In addition, growing obesity and DM in younger age groups has further undermined the improvements achieved in CVD. Diabetes and CVD share a'common soil'in their etiology and the causative factors for these diseases are termed as'cardiometabolic risk factors.'Cardiometabolic risk (CMR) is the global risk of developing type 2 diabetes and CVD. CMR factors include overweight or obesity, high blood glucose, HTN, dyslipidemia, inflammation and hypercoagulation, physical inactivity, smoking, age, race and ethnicity, gender, and family history. Among these, age, race/ethnicity, gender, and family history are non-modifiable risk factors. The remaining are modifiable risk factors and closely interrelated. Recently, systematic prospective studies have shown evidences that moderate lifestyle modifications help in reducing the metabolic risk factors. The major principles include cessation of smoking, enhanced physical activity, and reduction of excess weight. Healthy diet also has a major role in controlling overweight and maintaining ideal weight. Each of the risk factors poses a danger to good health; the propensity increases with multiple risk factors. It is also shown that the CMR factors tend to cluster as the metabolic syndrome. This book is designed to address such questions with supportive typical clinical scenarios, with which all readers will be able to identify. Thus it provides an excellent opportunity to widen one's perspective in this area.

Despite dizzyingly fast-paced advances over the past two decades, even the definition of Polycystic Ovarian Syndrome (PCOS) remains in dispute. Insulin Resistance and Polycystic Ovarian Syndrome: Pathogenesis, Evaluation, and Treatment highlights the recent transition of PCOS from an infertility disorder with a diagnosis based on ovarian tissue histology to a more complex clinical entity, a metabolic disorder in which insulin resistance plays a central role. With an expert panel of authors, each chapter provides an up-to-date and balanced overview of PCOS, paying special attention to the central role of insulin resistance in the syndrome's pathogenesis and in the management of its reproductive and metabolic abnormalities. Comprehensive and thought-provoking, Insulin Resistance and Polycystic Ovarian Syndrome: Pathogenesis, Evaluation, and Treatment is an invaluable resource for endocrinologists, gynecologists, and internists eager to learn more about this controversial and challenging disease.

Diabetes is now one of the major causes of morbidity worldwide. In many cases, the onset of diabetes is progressive, developing via a condition of insulin resistance. This book considers the development of this condition, its consequences and clinical and therapeutic aspects. The book reviews the normal biology of insulin action on glucose, lipids and proteins. It considers the pathological basis for insulin resistance in animal models and humans, and discusses the influence of heredity, dietary factors and exercise. Clinical consequences including dyslipidaemia, hypertension and polycystic ovary syndrome, and therapeutic strategies for treatment are also examined. • Provides an expert review of the phenomenon of insulin resistance • Brings together a host of recent research for the first time • Written by leading experts in biological and clinical research

Diabetes research on models comprising intact animal tissues, cell cultures and isolated pancreatic islets is essential for understanding the pathogenesis of the disease as well as the mechanisms responsible for the chronic complications associated with it. Enormous advances in the understanding of the development of diabetes and its prevention have recently been derived from work with such animal models. This book presents the state-of-the-art knowledge in the field of diabetes research directed at understanding the mechanisms governing the development of skeletal muscle insulin resistance. Muscle Metabolism will be of significant interest for those researching diabetes at an experimental level in both academia and the pharmaceutical industry. In addition, it will also be of interest to researchers in the fields of obesity, metabolism, endocrinology and molecular biology.

Insulin resistance, defined as a reduced biological action of insulin, has emerged as a major factor in the development and progression of a number of common non-communicable diseases in man. The role of insulin resistance in the aetiology of type 2 diabetes is particularly well-established. However, insulin resistance has also come to be regarded as a key component of a broader syndrome of common metabolic defects that conspire to increase the risk of atherosclerotic coronary heart disease. The ramifications of insulin resistance now embrace many different medical specialties. The objective of this book is to summarize the current state of knowledge about insulin resistance. Section 1 (Pathophysiology of Insulin Resistance) considers the development of current concepts of insulin resistance. This is followed by a critical review of techniques for the assessment of insulin action in humans. The section concludes with an outline of current hypotheses concerning the molecular defects responsible for insulin resistance. Section 2 (Insulin Resistance in Clinical Medicine) broadens the discussion to include physiological and pathological conditions with which insulin resistance is associated; the effects of drug treatment on insulin sensitivity are also considered. Section 3 (Management of Insulin Resistance and Associated Conditions) focuses on the avoidance and treatment of insulin resistance in its clinical manifestations. A discussion of the potential benefits of non-pharmacological measures prefaces a review of the range of drugs used in the treatment of type 2 diabetes and related disorders. References are confined to key articles at the end of each section. Improved nutrition allied to increased levels of physical exercise are of crucial importance in the battle to stem the increasing incidence and prevalence of insulin resistance; however, translation of such advice into action has proved difficult in practice. Thus, other approaches have been explored. Recent years have witnessed considerable progress in the pharmacological management of insulin resistance. In particular, the thiazolidinediones (and other insulin-sensitizing drugs) appear to provide a more specific assault on insulin-resistance. Clinical experience with these agents remains relatively limited and serious hepatotoxicity has clouded the first agent in this class - troglitazone. With its introduction into the USA in 1995 and driven by the publication of the United Kingdom Prospective Diabetes Study, metformin has enjoyed a renaissance. This well-established agent is finding application for new clinical indications. In parallel, the development of anti-obesity drugs continues apace. The molecular and genetic mechanisms underlying some forms of insulin resistance are being revealed. Original intellectual concepts such as the fetal origins hypothesis are challenging traditional views about the aetiology of insulin resistance and its clinical sequelae. These exciting scientific advances notwithstanding, the evolving global epidemic of obesity and type 2 diabetes represents an enormous public health challenge. Now more than ever, research must focus on identifying solutions that are applicable on the level of entire populations. By definition, these must also be practical and cost-effective.

Diabetes research on models comprising intact animal tissues, cell cultures and isolated pancreatic islets is essential for understanding the pathogenesis of the disease as well as the mechanisms responsible for the chronic complications associated with it. Enormous advances in the understanding of the development of diabetes and its prevention hav

Explains how to reverse the effects of Syndrome X--an ailment brought on by excessive consumption of processed high-carbohydrate foods.

Gerald Reaven, the discoverer of Syndrome X, and a panel of world-class investigators thoughtfully summarize our current understanding of how insulin resistance and its compensating hyperinsulinemia play a major role in the pathogenesis and clinical course of high blood pressure and cardiovascular disease-the so-called diseases of Western civilization. These distinguished authorities detail, for the first time, the pathophysiological consequences and the clinical syndromes, excluding Type 2 diabetes, related to insulin resistance. They also examine the genetic and lifestyle factors that contribute to the wide differences in insulin action that exist in the population at large. Timely and authoritative, Insulin Resistance: The Metabolic Syndrome X illuminates the full importance of insulin resistance as a major cause of hypertension, heart disease, and polycystic ovary syndrome.