作者: P.S Widdowson , R Upton , L Henderson , R Buckingham , S Wilson
DOI: 10.1016/S0006-8993(97)81680-0
关键词:
摘要: Neuropeptide Y (NPY) potently induces feeding, reduces thermogenesis and obesity in rats when injected into the cerebral ventricles. Groups of male Wistar were either restricted to 60% their normal daily food intake over 10 days or made obese by presenting them with a high-calorie diet rich sugars fat 6 weeks. Food lost up 20% body weight, compared control had large reductions mass. By contrast, dietary-induced weighed 26% more than controls due mainly increased Quantitative receptor autoradiography demonstrated reduced [(125)I]PYY binding hypothalamic lateral (perifornical) dorsal areas, ventromedial, arcuate dorsomedial nuclei, hippocampal CA3 region, centromedial amygdaloid nucleus thalamic paraventricular reuniens nuclei dietary controls. regional was significantly medial versus Masking NPY Y1 receptors 1 microM BIBP3226, selective antagonist, revealed that changes brains food-restricted dietary-obese BIBP3226-insensitive sites, presumably Y2 Y5 receptors. These data suggest dietary-restriction stimulates release resulting down-regulation 'feeding' and/or BAT thereby providing an drive eat restore caloric whilst reducing order conserve reserves. up-regulation is consistent inhibition hypothalamus, amygdala thalamus. Overall, we there increase during negative energy balance, such as food-restriction positive hyperphagia associated development obesity.