| Abstrakt: |
It has been established that the first transmitters of biological action of leptin in neurons of hypothalamus are neuropeptide Y (NPY) and α-melanocyte stimulating hormone ( α-MSH), as well as the agouti-related protein (AGRP) that is an antagonist of α-MSH and competitively inhibits binding of α-MSH to melanocortin receptors in the brain. Later, other transmitters of leptin, melanin concentrating hormone (MCH) and a transcript regulated by cocaine and amphetamine (CART), were studied. Leptin, on one hand, suppresses gene expression and biosynthesis of NPY, AGRP, and MCH in neurons that stimulate appetite, but, on the other hand, activates expression of (-MSH and CART genes in other neurons, which reduce food consumption. In the same neurons of arcuate nucleus, NPY and AGRP that stimulate food consumption are expressed, whereas in its other neurons there are coexpressed proopiomelanocortin (POMC), α-MSH, and CART that reduce appetite. Leptin stimulates expression of the SOCS3 gene in neurons participating in regulation of physiological functions and feeding behavior. SOCS3 blocks transduction of leptin hormonal signal by binding to phosphotyrosine of Janus kinase-2 (JAK2) on the receptor and thereby suppresses the tyrosine kinase activity of JAK2, which is needed for phosphorylation of STAT3 (signal transducer and activator of transcription). Since STAT3 participates in regulation of transcription of the genes, whose expression is controlled by leptin, inhibition of its phosphorylation blocks biological action of leptin in neurons. [ABSTRACT FROM AUTHOR] |
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