Insulin Resistance Pathophysiology

Glucose is one of the body's most important sources of energy. Glucose is absorbed from the blood into cells where it provides energy for a range of cellular functions. This cellular uptake of glucose is facilitated by the hormone insulin, which is secreted by the beta cells of the pancreas. Insulin also helps convert excess glucose into glycogen for storage in the liver.

In people with insulin resistance, the muscles, fat and liver cells fail to respond to insulin in this way and glucose remains in the blood rather than being taken up, even when insulin levels are raised. Instead, the triglycerides in fat or adipose cells are broken down to provide free fatty acids as the energy source.

Failure of liver cells to respond to insulin by converting glucose to glycogen, means glycogen stores are also decreased.

As the glucose remains in the blood rather than being taken up and used, hyperglycemia or a raised blood glucose level results. This hyperglycemia triggers the beta cells to produce even more insulin, raising the level of insulin further still.

This insulin resistance and hyperglycemia can lead to type 2 diabetes and metabolic syndrome. Metabolic syndrome is characterized by an excess distribution of abdominal fat, high blood pressure, raised levels of blood cholesterol and triglycerides and decreased levels of good cholesterol or high density lipoprotein (HDL) cholesterol. Together, these symptoms increase the risk of cardiovascular disease and stroke.

A variety of genetic and environmental factors are thought to raise the risk of insulin resistance but being overweight and physically inactive are major causative contributors.

Insulin Resistance Pathophysiology

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