Download Antidiabetic Agents: Recent Advances in their Molecular and by H.P.T. Ammon, H.U. Häring, M. Kellerer, H. Laube, L. PDF

By H.P.T. Ammon, H.U. Häring, M. Kellerer, H. Laube, L. Mosthaf, E.J. Verspohl and M.A. Wahl (Eds.)

Quantity 27, the 1st thematic quantity within the sequence, offers an summary of current wisdom with reference to the pharmacological and medical points of antidiabetic medications. It goals to stimulate extra attention of attainable options within the improvement of latest antidiabetic medications.

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Extra resources for Antidiabetic Agents: Recent Advances in their Molecular and Clinical Pharmacology

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In Europe and North America the ratio of undiagnosed to diagnosed cases may be as high as 1:1. Specific criteria have been adopted by WHO (1985a) for the diagnosis of Type-II diabetes mellitus. Concordance rates among monozygotic twins range from 55% to 100% compared with 17% in dizygotic twins. Type-II diabetes predisposition is best described as dependent on the inheritance of a single major gene in a co-dominant manner. Type-II diabetes is often associated with normal or high levels of circulating insulin, the absence of distinct HLA, insulin antibodies (lAB) and spontaneous ketoacidosis.

Ras contains an endogenous GTPase activity which inactivates the complex to Ras-GDP. This endogenous GTPase activity is again modulated by other proteins like GTPase-activating protein (GAP) or NF1. , 1993b). , 1993a). It is at present unclear whether this pathway is only involved in the generation of mitogenic signals by the insulin receptor or whether this coupling to a serine kinase MECHANISMS OF INSULIN ACTION 39 cascade is also involved in modulation of key enzymes of cell metabolism such as glycogen synthase.

A normal rate of HGP, however, in the presence of fasting hyperglycaemia, and a plasma insulin concentration nearly twofold greater, demonstrates that a latent hepatic resistance to the suppressive action of insulin is already present early in the course of NIDDM. HGP still remains within normal range because of the suppressive effect of hyperglycaemia. Tissue glucose uptake, however, is markedly reduced. In diabetic subjects, the glucose uptake of muscle tissue is delayed and retarded. While in control subjects muscle glucose uptake accounts for 75% of the total glucose uptake, normal-weight NIDDM patients have a 50% reduction in insulin-mediated peripheral glucose uptake.

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