Insulin is synthesized and secreted by Beta-cells of the pancreatic islets in response to glucose and other secret-agogues such as amino acids.
The secretion of insulin is very tightly matched to circulating glucose concentrations.
The response of the cells to insulin varies from individual to individual. In many cases the phrase insulin resistance describes a decrease in the ability of insulin to stimulate whole body glucose disposal.
This means that even with adequate levels of insulin, the glucose uptake into cells and tissues is not optimal.
Berson and Yalow in 1970 identified insulin resistance as ‘a state in which greater than normal amounts of insulin are required to elicit a quantitatively normal response.’
The impact of insulin resistance on glucose metabolism has wide implications for human disease, such as the development of type 2 diabetes, obesity hypertension, athermanous cardiac and vascular diseases, dyslipidemia and polycystic ovarian disease as well as other numerous pathological and physiological states.
The most common underlying of insulin resistance mechanism proposed is increased free fatty acids from abdominal fat in individuals with central obesity.
This lead to deranged insulin signaling, reduced muscular glucose uptake, increased triglyceride synthesis, and hepatic gluconeogenesis.
The meaning of insulin resistance
