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Clinical Gems

Our clinical gems come from the top selling medical books, and text books because knowledge is everything when it comes to diabetes.

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #59: Mechanisms of insulin signal transduction Part 3 of 8

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Insulin receptor substrate molecules -- receptor substrate/docking protein: Following insulin binding and receptor autophosphorylation, the next committed step in signal transduction is tyrosine phosphorylation of intracellular proteins. To accomplish this, autophosphorylation of the beta subunit mediates noncovalent but stable interactions between the receptor and intracellular substrate proteins, and this positions these molecules for tyrosine phosphorylation by the activated insulin receptor kinase.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #58: Mechanisms of insulin signal transduction Part 2 of 8

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Insulin receptors, ligand binding: The insulin action sequence is initiated with specific binding to high-affinity receptors on the plasma membrane of target cells. The insulin receptor is a large transmembrane glycoprotein consisting of two alpha- and two beta- subunits that form a heterotetramer, as depicted in Figure 12.1. The insulin receptor is synthesized from a single gene as a polypeptide pro receptor comprised of alpha- and beta- subunit sequences in tandem.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #56: Incretin Physiology in Health and Disease Part 6 of 6

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Potential mechanisms of incretin dysfunction in type 2 diabetes: Various potential explanations have been expounded in order to explain the reduced incretin effect in type 2 diabetes. One obvious factor to examine was the secretion of GIP and GLP-1. Regarding GIP, a number of studies have compared postprandial plasma concentrations between patients with and without diabetes. These studies have revealed increased, normal, or reduced GIP levels in patients with diabetes. Considering all studies together, there does not appear to be a general defect in GIP secretion. If anything, a slight increase in postprandial GIP levels might occur in patients with early type 2 diabetes, but clearly the differences in GIP levels would not sufficiently explain any alterations in insulin of glucose concentrations.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #54: Incretin Physiology in Health and Disease Part 4 of 6

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Central nervous effects: A role for GLP-1 in the central nervous regulation of food intake has been inferred from the high density of GLP-1 receptors in the hypothalamus. Also, direct intracerebroventricular administration of GLP-1 has caused a significant reduction in food intake in rats, and these actions could be abolished by co-administration of the GLP-1 receptor antagonist exendin.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #52: Incretin Physiology in Health and Disease Part 2 of 6

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Secretion of incretin hormones: The mucosa of the intestinal tract harbors a large number of endocrine cells that give rise to various peptide hormones. These include cholecystokinin, motilin, secretin, gastrin, gastric inhibitory polypeptide (GIP, also referred to as glucose-dependent insulinotropic polypeptide), glucagon-like peptide 1 (GLP-1), glucagon-like peptide 2, and peptide YY.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #51: Incretin Physiology in Health and Disease Part 1 of 6

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The incretin effect in health: The idea that gastrointestinal factors contribute to the control of postprandial glucose regulation dates back to the beginning of the twentieth century, when Moore and colleagues reported reductions in glucosuria after the oral administration of gut extracts xin patients with juvenile diabetes. Even though it is questionable whether these glucose-lowering effects were really attributable to the incretin activity of the extract (which is unlikely, because most gastrointestinal peptide hormones are inactivated by the gastric acid), this report can be considered as the first description of an incretin-like effect.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #50: Biosynthesis, secretion, and action of glucagon Part 4 of 4

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Glucagon and diabetes: Plasma levels of glucagon have been found to be increased in all experimental and clinical forms of diabetes mellitus. This disturbance undoubtedly contributes to the hyperglycemia of the disease and excessive ketogenesis of diabetic coma. Numerous studies have shown that failure of glucagon suppression contributes to postprandial hyperglycemia in type 1 and type 2 diabetes.

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