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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #138: Pathogenesis of Type 2 Diabetes Mellitus Part 9

In summary, postbinding defects in insulin action primarily are responsible for the insulin resistance in T2DM. Diminished insulin binding, when present, is modest and secondary to downregulation of the insulin receptor by chronic hyperinsulinemia. In type 2 diabetic patients with overt fasting hyperglycemia, a number of postbinding defects have been demonstrated, including reduced insulin receptor tyrosine kinase activity, insulin signal transduction abnormalities, decreased glucose transport, diminished glucose phosphorylation, and impaired glycogen synthase activity. The glycolytic/glucose oxidative pathway is largely intact and, when defects are observed, they appear to be acquired secondary to enhanced FFA/lipid oxidation. From the quantitative standpoint, impaired glycogen synthesis represents the major pathway responsible for the insulin resistance in T2DM, and is present long before the onset of overt diabetes, that is, in normal glucose-tolerant, insulin-resistant prediabetic subjects and in individuals with IGT. The impairment in glycogen synthase activation appears to result from a defect in the ability of insulin to phosphorylate IRS-1, causing a reduced association of the p85 subunit of PI-3 kinase with IRS-1 and decreased activation of the enzyme PI-3 kinase.

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Stanley Schwartz 2018 Transcript

Transcript of our Exclusive Interview: Stanley Schwartz talks with Diabetes in Control Publisher Steve Free during the AACE 2018 convention in Boston about the changing classifications of diabetes, why we need to move beyond thinking in terms of type 1 and type 2, and the need for precision medicine in treating patients with all types of diabetes.

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