pathogenesis of type 2 diabetes (NIDDM)

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The pathogenesis of type 2 diabetes (NIDDM) is poorly understood. Whilst there is clearly a relative insulin deficiency due to a combination of increased insulin resistance and decreased insulin secretion the relative contributions of these two factors varies from individual to individual.

The beta cell mass is reduced by about a half in type 2 diabetes (NIDDM) and necroscopic studies show the presence of an islet amyloid polypeptide in a significant proportion of patients.

Insulin resistance is increased in the peripheral tissues dependent upon insulin for glucose uptake and in the liver where insulin inhibits hepatic gluconeogenesis. These changes in insulin resistance are multifactorial and, at present, far from fully understood.

Last reviewed 01/2018