Published 2010
by Boston, Elsevier in Amsterdam .
Written in English
Edition Notes
Description based on print version record.
| Statement | edited by Gerald Litwack |
| Series | Vitamins and hormones -- v. 84 |
| Contributions | ScienceDirect (Online service) |
| Classifications | |
|---|---|
| LC Classifications | QP572.I5 I52 2010eb |
| The Physical Object | |
| Format | [electronic resource] / |
| ID Numbers | |
| Open Library | OL25563326M |
| ISBN 10 | 0123815177, 0123815347 |
| ISBN 10 | 9780123815170, 9780123815347 |
| OCLC/WorldCa | 702115607 |
Prandial State–During feeding, nutrient absorption causes an increases in plasma glucose, resulting in release of incretins from the gut and neural stimuli that promote insulin secretion. Under the control of insulin, the liver, sekletal muscle and adipose tissue actively take up . Insulin: Promotes cell use of glucose and carbohydrate storage (mostly in skeletal muscle) Constantly secreted by the pancreas in response to blood glucose levels Stimulates glycogen synthesis in the liver Facilitates entry of amino acids into the cell. Incretins also stimulate insulin secretion. Pancreatic Endocrine Function. Insulin resistance, largely caused by obesity and physical inactivity, both precedes and predicts type 2 diabetes. The insulin resistance preceding type 2 diabetes is commonly referred to as the metabolic syndrome. The latter condition consists of a cluster of risk factors, which are thought to be either causes or consequences of insulin resistance. The resultant rise in [Ca2+]i triggers insulin secretion. Insulin secretion is also modulated by hormones and neurotransmitters. Incretins such as GLP-1 and GIP bind to Gs-coupled receptors and activate adenylyl cyclase (AC), which increases intracellular levels of cyclic AMP. cAMP activates both PKA and Epac2 to potentiate insulin secretion.
Gerald Reaven, the discoverer of Syndrome X, and a panel of world-class investigators thoughtfully summarize our current understanding of how insulin resistance and its compensating hyperinsulinemia play a major role in the pathogenesis and clinical course of high blood pressure and cardiovascular disease-the so-called diseases of Western civilization. The impact of bariatric surgery on insulin sensitivity and glucose tolerance has refocused interest in the role of gut-derived factors in the regulation of insulin secretion and action. The incretins, glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) are released from endocrine cells in the small intestinal. Physiology of incretins (GIP and GLP-1) and abnormalities in type 2 diabetes In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, Page 65 Mercredi, février Insulin resistance Insulin secretion mg/dL Fasting glucose Postprandial glucose Prior to diagnosis After diagnosis Adapted from Bergenstal et al. ; International Diabetes Center. Ominous Octet Increased glucagon secretion Decreased amylin, β-cell secretion 80% loss at dx Increase glucose production Increased lipolysis Decreased glucose.
"Principles of Diabetes Mellitus, Second Edition" is an important update to the comprehensive textbook first published in and reissued in It is written for physicians of all specialties who, on a daily basis, deal with an illness which has reached epidemic proportions. The book is . It increases the amount of circulating incretins, which stimulate insulin secretion and inhibit glucose production. Sitagliptin was approved by the US Food and Drug Administration (FDA) for use with diet and exercise to improve glycemic control in adult patients with type 2 diabetes. pdf marie claire [no ] du 01/03/ - ce que les hommes pensent des sex-toys -la rose marie claire continue / 20 stars pour sauver les petites filles -special maigrir - mode -peut-on tout pardonner -le vrai danger des ondes. Holscher, C. (). The role of GLP-1 in neuronal activity and Vitamins and Hormones: INCRETINS AND INSULIN SECRETION (Vol. 84, pp. ).Elsevier.
