Insulin Resistance Calculator 1.0

Type 2 diabetes primarily develops from pathogenic defects in the mechanisms of insulin secretion and hepatic and peripheral insulin action. The consequent disruption of normal glucose metabolism involves a number of organ systems and is ultimately manifested in fasting and daytime hyperglycemia. Chronically elevated blood glucose concentrations determine the progression of the disease by further exacerbating insulin resistance and causing beta-cell exhaustion in addition to decreasing their responsiveness to glucose. The beta-cell secretory dysfunction is characterized by the lack of the early phase of glucose-induced insulin secretion and the insufficient and delayed late phase of secretion. Glycemic levels in patients with type 2 diabetes are directly related to the risk of developing microvascular and macrovascular complications, the main cause of the morbidity and mortality associated with this disease. The goal of treatment is to decrease the risk and delay the progression of these complications by improving glycemic control. Current oral antidiabetic agents, used as monotherapy or in combination, include traditional insulin secretagogues, insulin sensitizers and inhibitors of carbohydrate absorption. A greater understanding of the pathophysiology of type 2 diabetes and recent findings on the significance of meal-related glycemia to overall glycemic control are expanding the therapeutic options for treating this disease. A number of clinical tests have been developed to assess insulin sensitivity and beta cell function in vivo. Early diagnosis of insulin resistance at the early stage of disease is a prerequisite for effective prevention of its unfavorable sequelae, including reduction of cardiovascular morbidity and mortality. In 1985 a homeostatic model was developed for the assessment of insulin resistance aka HOMA. It was based on feedback dependence between fasting serum concentrations of insulin and glucose in blood and correlated well with data obtained using the isoglycemic glucose clamp. This program is based on the derivations of those studies.