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Insulin sensitivity

FIGURE 1 Hyperbolic relationship between beta-cell function and insulin sensitivity. In subjects with normal glucose tolerance a quasi-hyperbolic relationship exists between beta-cell function and insulin sensitivity. With deviation from this hyperbola, deterioration of glucose tolerance. Abbreviations: IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2DM, type 2 diabetes mellitus.

insulin resistance (with increased hepatic glucose production) is the driving force of hyperglycemia of type 2 diabetes.

Insulin resistance is strongly associated with obesity for which several mechanisms have been invoked. A number of circulating hormones, cytokines and metabolic fuels, such as nonesterified (free) fatty acids (NEFA) originate in the adipocyte and diminish insulin action (see below). In obese subjects, adipocytes are large, which renders them resistant to the ability of insulin to suppress lipolysis, especially in visceral or deep subcutaneous fat. This results in elevated release and circulating levels of NEFA and glycerol, both of which aggravate insulin resistance in skeletal muscle and liver (Fig. 2) (8).

production

FIGURE 2 Schematic representation of normal effects of insulin. Insulin secretion from the pancreas normally reduces glucose output by the liver, enhances glucose uptake by skeletal muscle, and suppresses fatty acid release from fat tissue.

production

FIGURE 2 Schematic representation of normal effects of insulin. Insulin secretion from the pancreas normally reduces glucose output by the liver, enhances glucose uptake by skeletal muscle, and suppresses fatty acid release from fat tissue.

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