Pathophysiology

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Insulin resistance and insulin secretion in type 2 diabetes mellitus

Glucose homeostasis is maintained by a delicate balance between insulin secretion from the pancreatic beta cells and insulin sensitivity of the peripheral tissues (eg, muscle, liver, and adipose tissue) [40]. In healthy individuals, the relationship between insulin sensitivity and secretion is nonlinear and best described by a hyperbolic function [40], which indicates that the product of insulin sensitivity and beta-cell function is constant for a given glucose tolerance in any one individual. This hyperbolic relationship implies that a feedback loop governs the interaction between the beta cells and the peripheral tissues. When insulin sensitivity decreases, insulin secretion must increase for glucose tolerance to remain constant (Fig. 1) [41]. An impairment in this compensatory increase in insulin secretion paves the way to glucose intolerance.

Decreased insulin sensitivity and impaired beta-cell function are the two key components in T2DM pathogenesis based on long-term experience in adults [41,42]. The sequence of development of these abnormalities has been debated extensively. The concept of "insulin insensitivity'' in DM originally was described by Himsworth in 1936 [43]. Further studies in adults documented that resistance to insulin-stimulated glucose uptake is a characteristic finding in patients who have T2DM and impaired glucose tolerance (IGT) [44]. Several studies in adults proposed that insulin resistance with compensatory hyper-insulinemia is the initial step in T2DM pathogenesis [18,41]. The subsequent step in T2DM pathogenesis is impairment in early insulin secretion, which initially leads to postprandial and later fasting hyperglycemia, at which time clinical DM becomes evident. This sequence also has been documented by

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