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Dołączył: 21 Lut 2011
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 Wysłany: Wto 14:09, 15 Mar 2011 Temat postu: ghd italia koi zme ssyl dho |
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Obesity-related hormones and the regulation of food intake
U. FA was concerned that the learning function, obesity,[link widoczny dla zalogowanych], diabetes, arteriosclerosis and other mechanism of action elucidated. Membrane lipid composition of the central nervous system is the basic n. 3, n-6 fatty acids in the origin of the composition of long chain PUFA. Is particularly important that LA synthesized by the AA, DHA (C22: 6n-3). In the absence of dietary n-3 fatty acids in rat brain, although DHA is low,[link widoczny dla zalogowanych], the brightness discrimination learning ability is low, but this time not only the restoration of brain DHA, but also not to AA and other long-chain n-6 series PUFA reduced, otherwise the learning capacity is not restored. Dietary n-6/n-3 ratio, the Japanese are 4.0-8.5. Greenland Eskimos Island is 0.36,[link widoczny dla zalogowanych], marine n-3 fatty acid intake was low in the U.S. and Europe who are very high value. Dietary fat tissue of LA for a long time in the accumulation of nuclear NPYmRNA LA is reduced, POMC, GALPmRNA rise. MRNA changes in the arcuate nucleus of which mode is similar to the thin cable to vote. Continuing to vote for intraventricular insulin receptor mRAN for antisense oligonucleotide in mice (IR.AS) and insulin play a role in the hypothalamus required for mouse IRS-2 deficient (IRS-2 ') have emerged feeding and insulin resistance in hyperthyroidism. These animals have arcuate nucleus NPY / AgRPmRNA rise, POMCmRNA reduce the tendency. That the role of insulin in the brain, and leptin, as are the NPY, POMC neurons mediated. Furthermore,[link widoczny dla zalogowanych], insulin and leptin in a way has the same intracellular cascade (c ~ cMe) reaction. On the other hand, continued to secrete leptin, and insulin secretion was increased briefly after the feeding, which secrete different forms, making the feeding inhibitory effect of insulin lower than leptin. The difference between the role of the arcuate nucleus alone current research is unable to explain. Insulin delivery was found to have increased after the MCHmRNA, so that the feeding inhibition of Insulin and leptin may also be differences in MCH neurons and the role of the different relevant. Physiological role of insulin and the different thin tangled, yet to be changes in levels of neurotransmitters to clarify. Fourth, ghrellnghrdln the stomach, intestines, pancreas, a synthetic peptide with growth hormone secretion and feeding the role of hyperthyroidism. ghrelln receptors are widely distributed in the hypothalamus, of which the arcuate nucleus NPY neurons in common. Intraventricular dosing ghrdin, arcuate nucleus NPY / AgRPmRNA increased expression, it can be activated individually isolated arcuate nucleus NPY neurons. So that the NPY neurons mediate the role of ghrelin. ghrelin activation of NPY neurons, and leptin inhibited the NPY neurons, NPY neurons via both the common target for contrast regulation. On the inverse relationship between the two can also be blood from obese leptin concentrations increased gllre-lin concentration decreased levels of this hormone negative correlation seen. The study also found, ghrelin did not see after dosing on POMC, MCHmRNA expression,[link widoczny dla zalogowanych], which also tips ghrelin, leptin and insulin signaling exist independent pathway. Pending and future use of ghrelin receptor deficient mice ghrelln more in-depth research. Five other feeding-related hormones pYY [3-36] is the digestive tract and feeding inhibition of pancreatic secretion of a hormone. p. YY [3-36] receptors exist in the arcuate nucleus Y2 receptors in NPY neurons in the presynaptic membrane, so that the main function is to regulate NPY neurons. In the POMC 'mice and MCAR mice. Cast to the feeding inhibitory effect of leptin could be caused by weakened, and p. YY [3-36] the effect is not diminished, so the role of POMC neurons of p. YY [3-36] effects may not be necessary. In addition, Y2 receptor-deficient mice (Y2.), Although feeding hyperthyroidism, but the arcuate nucleus NPY / AgRPmRNA POMCmRNA expression and low expression of hyperthyroidism was not significant; and CARTmRNA and paraventricular nuclei CRHmRNA was significantly reduced. This abnormal mRNA is different from the observation of leptin or insulin receptor abnormalities seen in mice. CCK is secreted by the duodenum of a feeding inhibiting hormone vagotomy. Peripheral CCK given time. Inhibitory effect is not observed feeding, so that the origin of the small intestine by vagal fibers to the heart of signal transduction mediated by CCK in feeding inhibition. That it is through the inhibition of the hypothalamic dorsomedial nucleus, NPY neurons to produce feeding inhibition. Fumihiko Maekawa and so on. New Medicine, 2004,59 (9): 117. Translation Daimei Feng Zhao United States Mi
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