Insuhn secretion

In starvation, glucose must be ptovided for the brain and erythrocytes initially, this is supphed from hver glycogen reserves. To spare glucose, muscle and other tissues reduce glucose uptake in response to lowered insuhn secretion they also oxidize fatty acids and ketone bodies preferentially to glucose. 

Insuhn, secreted by the p cells of the pancreas in response to rising blood glucose levels, is a signal that glucose is abundant. It s saying,... 

Gallbladder and ducts Contraction p Insuhn secretion Relaxation... 

Shoesmith Berke SJ, Flores Schmied FA, Brunt ER, Ellerby LM, Paulson HL (2004) Caspase-mediated proteolysis of the poly glutamine disease protein ataxin-3. J Neurochem 89 908-918 Smith R, Bacos K, Fedele V, Soulet D, Walz HA, Obermuller S, Lindqvist A, Bjdrkqvist M, Klein P, Onnerfjord P, Brandin P, Mulder H, Li JY (2009) Mutant huntingtin interacts with P-tubuUn and disrupts vesicular transport and insuhn secretion. Hum Mol Genet 18 3942-3954 Spindler M, Beal MF, Henchcliffe C (2009) Coenzyme QIO effects in neurodegenerative diseases. Neuropsychiatr Dis Treat 5 597-610... 

Tze WJ, Tai J, Murase N, Tzakis A, Starzl TE. Effect of FK 506 on glucose metabolism and insuhn secretion in normal rats. Transplant Proc 1991 23(6) 3158-60. 

Pathogenesis of Type 1 Diabetes Mellitus Type 1 diabetes mellitus results from a cellular-mediated autoimmune destruction of the insuhn-secreting cells of pancreatic p-cells. In the vast majority of patients, the destruction is mediated by T cells. This is termed type lA or immune-mediated diabetes (Box 25-2). The a-, 8-, and other islet cells are preserved. The islet cells have a chronic mononuclear cell infiltrate, called insulitis. The autoimmune process leading to type 1 diabetes begins months or years before the clinical presentation, and an 80% to 90% reduction in the volume of the j3-cells is required to induce symptomatic type 1 diabetes. The rate of islet cell destruction is variable and is usually more rapid in children than in adults. 

A shift of phosphate from extracellular fluid to intracellular fluid is a common cause of hypophosphatemia. A major etiology of low serum phosphate is carbohydrate-induced stimulation of insuhn secretion, which increases the transport of glucose and phosphate into insulin-sensitive cells, where it is incorporated into sugar phosphates and ATP. Oral or intravenous carbohydrate and injected insuhn decrease serum phosphate. Refeeding of malnourished individuals creates an anabohc state, causing an intracellular shift of phosphate. Respiratory alkalosis leads to an increase in intracellular pH, which activates phosphoffuctokinase and accelerates glycolysis, causing a shift of phosphate into the cell. 

Straub, S. G., Yajima, H., Komatsu, M., Aizawa, T., Sharp, G. W. G. (2002). The effects of cerulenin, an inhibitor of protein acylation, on the two phases of glucose-stimulated insuhn secretion. Diabetes 51(Suppl 1) S91-S95. 

The effects of glucocorticoids on glycogen accumulation appear to be predominantly, although not exclusively, insulin-dependent, as glycogen accumulation is markedly reduced in pancreatectomized animals. Glucocorticoid-stimulated increases in insuhn secretion promote further glycogen accumulation. 

Ca of a period of the order of 2 min have been reported (Valdeolmillos et al, 1989) their link with insuhn secretion remains to be estabUshed. 

Reaven GM, Hollenbeck CB, Chen Y-DI. Relationship between glucose tolerance, insuhn secretion, and insulin action in non-obese individuals with varying degrees of glucose tolerance. Diabetologia 1989 32 52-55. 

Kim SH, Abbasi F, Chu, et al. Rosiglitazone reduces glucose-stimulated insuhn secretion and increases insuhn clearance in nondiabetic, insulin resistant individuals. Diabetes 2005 54 2447-2452. 

Kjems LL, Holst JJ, Vplnnd A, Madsbad S. The influence of GLP-1 on glncose-stimulated insuhn secretion effects on beta-cell sensitivity in type 2 and nondiabetic snbjects. Diabetes 2003 52 380-386. 

Transit of food from the stomach along the bowel has stimulatory effects on incretins, which regulate insuhn secretion and beta-cell regeneration as well as glucagon release. 

GH-RIH inhibits basal secretion of insulin and glucagon (C2, Dl, G2, Mil), glucose-stimulated insuhn secretion (Al) and arginine- stimulated glucagon secretion (Mil), and the insulin and glucagon response to a meal and to the administration of tolbutamide (G4) (Figs. 17-19). 

However, when both drugs were applied together, the Katp channels were almost completely closed. Dramatic inhibition of Katp channels is sufficient to cause membrane depolarization in the pancreatic beta cells and stimulate insuhn secretion. 

Chronic exposure to fi-ee fatty add reduces pancreatic beta cell insulin content by increasing basal insuhn secretion that is not compensated for by a corresponding increase in proinsulin biosynthesis translation. 

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