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Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 149))

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Abstract

Type 2 diabetes (formerly known as non-insulin-dependent diabetes mellitus (NIDDM) or adult onset diabetes) is characterized by peripheral insulin resistance, increased hepatic glucose production, and defects in insulin secretion from pancreatic β-cells (DEFRONZO 1988). In skeletal muscle, the tissue responsible for up to 90% of insulin-stimulated glucose disposal, both oxidative and non-oxidative glucose utilization is impaired (DEFRONZO 1988). The increase in hepatic glucose production is associated with increased levels of glucagon and an increased utilization of peripherally derived three carbon gluconeogenic precursors, the latter of which may be due to skeletal muscle insulin resistance (MOLLER 1993). The β-cell dysfunction is due to multiple defects including blunted responses to glucose, changes in insulin secretory patterns, and secretion of incompletely and partially processed insulin (POLONSKY 1995). Although the underlying cause of these defects in the majority of patients with NIDDM is unknown, there is a strong correlation with obesity, especially centripetal obesity (BODEN 1997).

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Burant, C.F. (2000). Insulin Sensitization. In: Lockwood, D.H., Heffner, T.C. (eds) Obesity: Pathology and Therapy. Handbook of Experimental Pharmacology, vol 149. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59651-3_15

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