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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 #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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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #49: Biosynthesis, secretion, and action of glucagon Part 3 of 4

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Control of glucagon release: There is considerable evidence that the control of glucagon secretion is multifactorial and involves direct effects of nutrients on alpha-cell stimulus-secretion coupling as well as paracrine regulation by insulin, somatostatin and, possibly, other mediators such as zinc, γ-amino-butyric acid (GABA) or glutamate. Glucagon secretion is also regulated by circulating hormones and the autonomic nervous system.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #48: Biosynthesis, secretion, and action of glucagon Part 2 of 4

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Physiologic effects of glucagon: Glucagon acts through binding to specific receptors located at the target cell plasma membrane. The major common effect of glucagon is to activate adenylate cyclase and to increase the intracellular production of cAMP. There is considerable evidence that binding of glucagon to its receptor activates an intermediate transduction process that involves the participation of guanosine triphosphate (GTP), divalent cations, and adenosine (or other similar natural substances).

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #47: Biosynthesis, secretion, and action of glucagon Part 1 of 4

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Glucagon, discovered in 1923 as a contaminant of early insulin preparations, has long been a neglected hormone. Glucagon was among the very first polypeptide hormones to be isolated, purified, sequenced, and synthesized. Thanks to the pioneering work of Unger, it was the first polypeptide hormone to become measurable by radioimmunoassay, almost one year before insulin. It has served two Nobel Prize winners as a unique tool, which permitted Sutherland and his associates to discover cyclic AMP (cAMP), and Rodbell and his coworkers to discover the role of G-proteins in cell-membrane receptors.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #46: Neuropeptides and Islet Hormone Secretion Part 5 of 5

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Summary of present-day knowledge: We know today that the pancreatic islets are innervated by parasympathetic, sympathetic, and sensory nerves. The parasympathetic nerves stimulate insulin and glucagon secretion whereas sympathetic nerves inhibit insulin secretion and stimulate glucagon secretion; the net influence of the sensory nerves is not yet clearly established.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #45: Neuropeptides and Islet Hormone Secretion Part 4 of 5

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Sympathetic effects and mediation: Sympathetic nerves inhibit insulin and stimulate glucagon secretion. Their activation may help mediate stress-induced changes in islet hormone secretion including the glucagon counterregulatory response to hypoglycemia.These effects may be mediated by the combination of the classical neurotransmitter noradrenaline and the sympathetic neuropeptides (galanin and NPY). All three neurotransmitters can inhibit insulin and stimulate glucagon secretion, thus mimicking the effects of sympathetic activation on islet hormone secretion. In addition, galanin and NPY meet several other of the criteria needed to be classified as a physiologic neurotransmitter.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #44: Neuropeptides and Islet Hormone Secretion Part 3 of 5

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Islet sympathetic nerves: Islets are densely innervated by sympathetic nerves, as demonstrated by fluorescence microscopy, electron microscopy, and immunocytochemistry. The islet sympathetic nerves are postganglionic nerve fibers with most nerve cell bodies located in the celiac ganglion and some in the paravertebral sympathetic ganglia. Electrical activation of the sympathetic nerves inhibits insulin secretion and stimulates glucagon secretion.

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