Insulin release stimulation

Galanin GAL1 Human cDNA Alzheimer s disease, feeding diabetes, growth disorders, pain, stroke, obesity, Parkinson s disease Inhibition of acetylcholine release, regulation of motility, inhibition of insulin release, stimulation of growth hormone, inhibition of LH-RH secretion... 

Insulin release stimulation. Fruit-fixed oil, in cell culture, was active on pancreatic islets Decoction of the dried leaf, in cell culture at a concentration of 0.4 pg/mL, was active on adrenal gland . ... 

Diagrammatic representation of insulin secretion from pancreatic fi cells. The sequence of events of insulin secretion coupled to glucose entry into fi cells consists of glucokinase action, ATP production, inhibition of the ATP-sensitive K+ channel, membrane depolarization, Ca + influx, and insulin release. Neurotransmitters acetylcholine and norepinephrine stimulate and inhibit insulin secretion via trimeric G-proteins Gq and Gj, respectively. Glucagon-like peptide (GLP) promotes insulin release via the G-protein G. Sulfonamides and diazoxide have direct effects on sulfonylurea receptors (SURs) the former promotes insulin release and the latter inhibits insulin release. +, Stimulation —, inhibition. Other abbreviations are given in the text. 

Hepoxylins are metabolites of arachidonic acid which arise from 12-HPETE in tissues such as pancreatic islet cells (where they stimulate glucose-dependent insulin release) and brain (where they appear to have a neuromodulatory role). The structure of the hepoxylins was confirmed by synthesis which also has provided this scarce material for biological investigation. 

Prandial insulin releasers (meglitinides) Repaglinide, nateglinide Stimulate insulin secretion (rapid and short-acting < 6 h) Oral... 

Antidiabetic Drugs other than Insulin. Figure 1 Sulphonylureas stimulate insulin release by pancreatic (3-cells. They bind to the sulphonylurea receptor (SUR-1), which closes Kir6.2 (ATP-sensitive) potassium channels. This promotes depolarisation, voltage-dependent calcium influx, and activation of calcium-sensitive proteins that control exocytotic release of insulin. 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

Monotherapy with sulfonylureas generally produce a 1.5% to 2% decline in HbAlc concentrations and a 60 to 70 mg/dL (3.33-3.89 mmol/L) reduction in FBG levels. Secondary failure with these drugs occurs at a rate of 5% to 7% per year as a result of continued pancreatic p-cell destruction. One limitation of sulfonylurea therapy is the inability of these products to stimulate insulin release from (1-cells at extremely high glucose levels, a phenomenon called glucose toxicity. 

Nickel ions have been shown to depress the in vivo and in vitro release of prolactin [336], while the release of growth hormone was stimulated, and only at relatively high ion concentrations. Hyperglycemia occurs in rats following intraperitoneal or intratracheal injections of NiCl2 [265, 337, 338], The mechanism of action of nickel appears to be inhibition of insulin release this inhibition could be related to the extremely high concentration of nickel found in the pituitary and the effect on the secretion of the pituitary hormones (growth hormone and adrenocorticotropic hormone). 

Biosynthesis and degradation of glycosaminoglycans biosynthesis of collagen, mineralization and demineralization of bone. Fatty acid synthesis and triglyceride storage in adipocytes promoted by insulin and triglyceride hydrolysis and fatty acid release stimulated by glucagon and adrenaline (epinephrine). 

As discussed above, insulin suppresses the breakdown of triglyceride within fat cells in the post-prandial period, preventing release of fatty acids from adipocytes in healthy individuals. Insulin also stimulates triglyceride clearance from triglyceride-rich lipoprotein particles and the esterification of fatty acids to form the intra-adipocyte triglyceride store. 

Repaglinide is a newer oral hypoglycaemic agent, indicated in type 2 diabetes either in combination with metformin or as monotherapy. Repaglinide stimulates insulin release. 

Metformin, a biguanide derivative, can lower excessive blood glucose levels, provided that insulin is present Metformin does not stimulate insulin release. Glucose release from the liver is decreased, while peripheral uptake is enhanced. The danger of hypoglycemia apparently is not increased. Frequent adverse effects include anorexia, nausea, and diarrhea Overproduction of lactic acid (lactate acidosis, lethality 50%) is a rare, potentially fatal reactioa Metformin is used in combination with sulfony-lureas or by itself. It is contraindicated in renal insufficiency and should therefore be avoided in elderly patients. 

The biosynthesis and release of insulin by the pancreatic B cells (see p. 160) is stimulated by high blood glucose levels (> 5 mM). The insulin released then stimulates increased uptake and utilization of glucose by the cells of the muscle and adipose tissues. As a result, the blood glucose level falls back to its normal value, and further release of insulin stops. 

Acid glucan-Lq-a-glucosidase (mouse) Inhibition of enzyme activity by 0.3 mM HA with parallel inhibition of glucose-stimulated insulin release 58... 

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