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  Insulin resistance

Insulin is a polypeptide hormone secreted by the beta cells of the islets of Langerhans located in the pancreas. These endocrine cells are scattered throughout the parenchyma of the pancreas. The pancreas is the only organ which is both an endocrine and exocrine gland (an accessory digestive gland). The exocrine part secretes pancreatic enzymes namely: pancreatic amylase and lipase which aids in chemical digestion of food. The insulin produced by the beta cells is released directly into the blood stream and acts as a chemical messenger called hormones. This hormone reaches the target cells and acts on the receptors found along the cell membranes. The main actions of insulin are directed at controlling the metabolism of carbohydrates (e.g. sugars and starches), lipids (fats), and proteins.

Insulin resistance
Insulin resistance


Insulin resistance (IR) is a pathologic condition wherein the target cells of the body become resistant to the effects of insulin. In this case, even if you have normal levels of insulin in the body, the amount is still considered somehow insufficient to produce a normal response from the fat, muscle and liver cells (target cells). In short, there is decreased sensitivity of receptors along the cell membranes of the target cells to insulin. As a result, you need higher levels of insulin in order to achieve its beneficial effects on the body.

The following are the major effects of insulin resistance: hydrolysis of stored triglycerides or fats, which elevates free fatty acids (FFA) in the plasma; reduction of glucose uptake or glucose utilization among muscle cells and reduction of glycogenesis (glycogen formation) or decreasing glucose storage in the liver cells with both effects leading to elevation of blood sugar levels.

This theory of elevated plasma levels of insulin and glucose due to insulin resistance often leads to the metabolic syndrome and type 2 diabetes also known as non-insulin dependent diabetes mellitus.

Metabolic syndrome is a combination of symptoms due to the concomitant appearance of diabetes mellitus (type 2), hypertension (HPN), central obesity and combined hyperlipidemia defined as increased levels of triglycerides (fats) and low density lipoprotein (LDL) – the bad cholesterol and decreased levels of high density lipoprotein (HDL) – the good cholesterol. This syndrome may also be associated with polycystic ovarian disease. In obese patients especially those with high visceral fat, compensatory hyperinsulinemia causes the down regulation of the insulin receptors potentiated by the inherent defects within the target cells itself. Both aspects play a role in the development of insulin resistance.

Type 1 diabetes mellitus is also known as insulin dependent diabetes mellitus (IDDM) which is a frank hyperglycemia that develops as a result of absolute lack of insulin secreted by the pancreatic beta cells to maintain normal blood sugar levels also known as "euglycemia".

The following are the most commonly used diagnostic tools requested to confirm the presence of insulin resistance. First is the fasting Insulin Levels of greater than the upper limit (approximately 60pmol/L) which is considered to be a positive evidence of insulin resistance. Another is the Oral Glucose tolerance testing (OGTT), performed on a patient who fasted for at least 8 hours then consume a 75 gram oral dose of glucose followed by series of blood extraction wherein the blood glucose levels are then measured over the following 2 hours. A glucose level greater than or equal to 11.1mmol/L at 2 hours or greater than or equal to 7.0mmol/L fasting is diagnostic for diabetes mellitus. Lastly, the hyperinsulinemic euglycemic clamp, the gold standard for investigating and quantifying insulin resistance. This is considered to be the gold standard because it measures the exact amount of glucose necessary to compensate for an increased insulin level without causing hypoglycemia. However, this is rarely performed in the clinic setting. In medical research, this method of investigation is widely employed.

The exact cause of the majority of insulin resistance cases remains unknown. Associated conditions include: an abnormally sedentary lifestyle compounded by the effects of aging on the body or lack of physical exercise which can both lead to obesity; hemochromatosis ; polycystic ovarian syndrome (PCOS) ; hypercortisolism (e.g. Cushing syndrome due to steroid use or Cushing's disease); certain drugs such as rifampicin (RIF), isoniazid (INH), olanzapine, risperidone, progesterone derivatives, many antiretrovirals, possibly alcohol and genetic causes such as mutations of the insulin receptors.

The main treatment for insulin resistance is exercise and weight reduction. Exercise and diet were nearly as two times as effective as metformin, an oral antidiabetic drug at reducing the risk of progressing to type 2 diabetes mellitus. Dietary intake of more polyunsaturated fatty acids is also preferred than monounsaturated fatty acids (or unsaturated fats) because the former can increase insulin sensitivity in contrast to the latter which promote insulin resistance. Both metformin and the thiazolidinediones (oral anti-diabetic agents) may improve insulin resistance, but are only approved drugs of choice for type 2 diabetes and not for insulin resistance.

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