Type2 diabetes mellitus is characterized by a both combinations of inadequate insulin secretion by pancreatic beta cells and peripheral insulin resistance. Insulin resistance, which has been associate to proinflammatory cytokines in plasma and elevated levels of free fatty acids, it leads to decreased glucose transport into muscle cells, elevated hepatic glucose production, and increased breakdown of fat. The major role for excess glucagon cannot be underestimated; indeed, Type2 diabetes (T2D) is an islet paracrinopathy in which the reciprocal relationship between the insulin-secreting beta cell and the glucagon-secreting alpha cell is lost, which leads to hyperglucagonemia and hence the consequent hyperglycaemia. For type 2 diabetes mellitus (T2DM) to occur, both insulin resistance and inadequate insulin secretion must exist. Generally all overweight or obese individuals have insulin resistance, but diabetes develops only in those individuals who cannot raise insulin secretion to that level so that it can compensate for their insulin resistance. Their insulin concentrations may be high, which results in low level of glycaemia.
- Acute pancreatitis symptoms
- Identification of β-cell dysfunction and insulin resistance
- Differentiation of diabetes by pathophysiology, natural history
- Clinical features of diabetes mellitus
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