Insulin Resistance Ecab

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-α, 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.

India in particular and South-Asia in general have witnessed a rapid increase in the prevalence and incidence of cardiovascular disease over the past 25 years. Lifestyles changes, unhealthy diet, lack of regular physical exercise, and obesity have all led to rising prevalence of metabolic syndrome. It is of no wonder that metabolic syndrome is being increasingly recognized as a clinical entity which is believed to be associated with increased risk of cardiovascular disease beyond individual risk factors, though this is at times debated. This monograph addresses the total nuance of metabolic syndrome in its entirety and answers questions frequently asked on this subject. The authors are internationally respected investigators in their own right having made major contributions in the particular field and are revered teachers as well. The book itself has clear sections which makes it very user friendly and divided into two volumes. The first volume has the evaluation of metabolic syndrome and the vastness of the problem and how it leads to smouldering dysfunctional endothelium making such a patient vulnerable to vascular disease. It purely deals with clinical issues we face daily in metabolic syndrome and patients. It is fairly broad-based to answer most of the queries which arise in a busy clinician’s head while dealing with metabolic syndrome on a day-to-day basis. Of special interest are chapters on metabolic syndrome in children, non-alcoholic fatty liver disease and hypogonadism.

India in particular and South-Asia in general have witnessed a rapid increase in the prevalence and incidence of cardiovascular disease over the past 25 years. Lifestyles changes, unhealthy diet, lack of regular physical exercise, and obesity have all led to rising prevalence of metabolic syndrome. It is of no wonder that metabolic syndrome is being increasingly recognized as a clinical entity which is believed to be associated with increased risk of cardiovascular disease beyond individual risk factors, though this is at times debated. This monograph addresses the total nuance of metabolic syndrome in its entirety and answers questions frequently asked on this subject. The authors are internationally respected investigators in their own right having made major contributions in the particular field and are revered teachers as well. The book itself has clear sections which makes it very user friendly and divided into two volumes. The book rightfully deals with management of the syndrome and lays emphases not only on lifestyle measures (which are a cornerstone) but also judicious use of pharmacotherapy and also surgical techniques currently in use.

Critical Issues and Diabetes - ECAB - E-Book

Diabetes is one of the most important non-communicable lifestyle diseases. Diabetes is a multifaceted disorder which possibly influences and impacts body pathophysiology by different mechanisms and in varied ways. Diabetes has a very distinguished impact on cardiovascular system and plays a detrimental role in development of cardiovascular disorders. Metabolic memory is used to describe the impact of exposure to glucotoxicity, lipotoxicity and other metabolic disturbances, either as an adverse or a beneficial cell response which determines the later development of vascular complications. Terms such as metabolic imprint, legacy effect, glycemic memory or latent hyperglycemic damage are also used. Diabetes has significant impact on different facets of life. Diabetes has a distinguished but significant impact on development of various cancers. Diabetes has a positive, negative and even neutral impact on pathogenesis and progression of cancer depending upon the tumor site. On the contrary, cancer also has a significant effect on diabetes development and management. These facets tend to get overlooked in the study of diabetes development and management. All these aspects are being thoroughly covered in this project so as to facilitate better management of diabetics.

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.

Cell health depends on a steady supply of fuel from glucose and free fatty acids. Both these major fuels are regulated by insulin. Cells in the muscle, liver, and fat need insulin to receive glucose, and hence do not become exposed to high blood glucose levels when the blood sugars are high and insulin levels are low. The lack of insulin slows the movement of glucose into these cells, and probably spares them from damage when blood sugars are high. However, other cells such as those in the brain, nervous system, heart, blood vessels and kidneys pick up glucose directly from the blood without using insulin. These cells, except the brain, are more prone to damage from high blood sugars because they become exposed to high internal levels of glucose. This to quite an extent explains why damage tends to occur in specific organs such as in nerve and kidney cells, and in small blood vessels like those in the eyes. This project on the organ damage in diabetes is an attempt to elaborate on the various factors to be considered in managing these patients, the pointers for early diagnosis and prevention of the same.