Leptin is synthesized and secreted by white adipose tissue, by acting on hypothalamic nuclei it decreases appetite and\nincreases energy expenditure through sympathetic activation to decreases adipose tissue mass. Leptin also activate sympathetic\nnervous system in kidney, spleen, heart and hind limb. Leptin secretion decreases during fasting and increased after several\ndays of overfeeding to regulate energy balance. Leptin act on Ob-Rb receptor which is tyrosine kinase receptor and activate\nJAK/STAT pathway, PI3 kinase signaling pathway and Mitogen Activated Protein (MAP) kinas signaling. Leptin induced anorexic\neffect is mediated by synthesis of melanocyteââ?¬â??stimulating hormone in POMC neuron which act on MCR-3 and MCL-4 leptin\ninduced sympathetic activation is also mediated by STAT3 activation in propiriomeclanortin neuron. Released melanocyte\nstimulating hormone act on MCR-4 receptor. Most of obese human have high circulating leptin but remaining obese indicates\nresistance to anorexic and weight lowering effect of leptin. Leptin induce anorexic effect and sympathetic nervous system\nstimulatory effect is mediated by different area of brain. Thus leptin resistance is selective in obesity i.e. increased leptin level\nshows resistance to anorexic and weight lowering effect of leptin with preservation of sympatho activation. Although leptin\nstimulate renal SNS, acute administration of leptin does not significantly affect blood pressure because of release of NO and\nnatriuresis. But chronic hyperleptemia in obesity induces increased renal sympathetic activity and rise in BP by activation of\nNa+K+ATPase pump and inhibition of inhibitory effect of NO on Na+K+ATPase pump, which increases Na+ and water reabsorption\nand rise arterial blood pressure.
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