Insulin resistance glucose metabolism

Insulin resistance occurs when the normal response to a given amount of insulin is reduced. Resistance of liver to the effects of insulin results in inadequate suppression of hepatic glucose production insulin resistance of skeletal muscle reduces the amount of glucose taken out of the circulation into skeletal muscle for storage and insulin resistance of adipose tissue results in impaired suppression of lipolysis and increased levels of free fatty acids. Therefore, insulin resistance is associated with a cluster of metabolic abnormalities including elevated blood glucose levels, abnormal blood lipid profile (dyslipidemia), hypertension, and increased expression of inflammatory markers (inflammation). Insulin resistance and this cluster of metabolic abnormalities is strongly associated with obesity, predominantly abdominal (visceral) obesity, and physical inactivity and increased risk for type 2 diabetes, cardiovascular and renal disease, as well as some forms of cancer. In addition to obesity, other situations in which insulin resistance occurs includes... 

Abdominal obesity is associated with a threatening combination of metabolic abnormalities that includes glucose intolerance, insulin resistance, hyperinsulinemia, dyslipidemia (low HDL and elevated VLDL), and hypertension. This clustering of metabolic abnormalities has been referred to as syndrome X, the insulin resistance syndrome, or the metabolic syndrome. Individuals with this syndrome liave a significantly increased risk for developing diabetes mellitus and cardiovascular disorders. For example, men with the syndrome are three to four times more likely to die of cardiovascular disease. 

PPARy is a transcription factor which controls the expression of enzymes and proteins involved in fat and glucose metabolism. More importantly, stimulation of this receptor induces differentiation of preadipocytes to adipose cells. It is believed that the formation of additional, small fat cells lowers free fatty acids and hepatic triglycerides, thereby collecting insulin resistance. 

Diabetes is a metabolic disorder where glucose metabolism in the body is impaired. Type 1 diabetes is an early onset disease in which the pancreatic cells lose the function of insulin secretion either by genetic disposition or by a viral attack. Type 2 diabetes is a late onset disease developed due to insufficient insulin secretion or insulin resistance resulting in impaired glucose metabolism. 

ATP III recognizes the metabolic syndrome as a secondary target of risk reduction after LDL-C has been addressed. This syndrome is characterized by abdominal obesity, atherogenic dyslipidemia (elevated triglycerides, small LDL particles, low HDL cholesterol), increased blood pressure, insulin resistance (with or without glucose intolerance), and prothrom-botic and proinflammatory states. If the metabolic syndrome is present, the patient is considered to have a CHD risk equivalent. 

In both types of diabetes, however, this normal process malfunctions. A gland called the pancreas, found just behind the stomach, makes insulin. In people with insulin-dependent diabetes, the pancreas does not produce insulin at all. This condition usually begins in childhood and is known as Type I (formerly called juvenile-onset) diabetes. These patients must have daily insulin injections to survive. People with non-insulin-dependent diabetes usually produce some insulin in their pancreas, but their bodies tissues do not respond well to the insulin signal and, therefore, do not metabolize the glucose properly, a condition known as insulin resistance. 

A brief overview about the fundamental principles of the pathogenesis of skeletal muscle insulin resistance and its contribution to the development of type 2 diabetes mellitus is given in the following. Priority is given to the role of lipid metabolism, which is the main field of the reported spectroscopic studies. Furthermore, the technique of euglycemic hyperinsulinemic glucose clamp is described allowing determination of the individual insulin sensitivity of musculature. The role of IMCL in insulin resistance of the skeletal muscle is discussed. 

To gain further insight into the mechanisms involved in defective insulin-stimulated glucose uptake in skeletal muscle of insulin-resistant subjects, the possible role of IMCL in the pathogenesis of skeletal muscle insulin resistance and type 2 diabetes mellitus was explored by comparing insulin sensitivity (GIR) and IMCL content of insulin-resistant and insulin-sensitive offsprings of patients with type 2 diabetes. Twenty-six healthy subjects were included in the first study, 13 of them classified as insulin-sensitive and further 13 as insulin-resistant. Metabolic and anthropometric data are given in Table 4. 

There are limitations in the use of FDG for viability assessment. Normal myocardium (normal perfusion and normal metabolism) in diabetics may not take up FDG due to insulin resistance associated with elevated free fatty acids in blood. Consequently, there is no FDG uptake anywhere in the heart and the study is uninterpretable. Flowever, giving insulin intravenously at the time of glucose loading enhances myocardial uptake, reduces free fatty acids in blood, and provides diagnostic images. 

Defects in glucose uptake into muscle cells are characteristic of insulin resistance in type 2 diabetes and the metabolic syndrome. This phenomenon is likely to be due to reduced activity of a transporter that operates by what mechanism ... 

T Diabetes mellitus, caused by a deficiency in the secretion or action of insulin, is a relatively common disease nearly 6% of the United States population shows some degree of abnormality in glucose metabolism that is indicative of diabetes or a tendency toward the condition. There are two major clinical classes of diabetes mellitus type I diabetes, or insulin-dependent diabetes mellitus (IDDM), and type II diabetes, or non-insulin-dependent diabetes mellitus (NIDDM), also called insulin-resistant diabetes. 

The metabolic abnormalities of obesity reflect molecular signals originating from the increased mass of adipocytes. The predominant effects of obesity include dyslipidemias, glucose intolerance, and insulin resistance, expressed primarily in the liver, muscle, and adipose tissue. 

Carbohydrate metabolism was known at an early date to be affected by combined oral contraceptives. A mild to moderate degree of insulin resistance was found in some investigations (167,168). However, the considerably impaired glucose tolerance described in some users in... 

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