Evidence that neurotensin mediates the central effect of leptin on food intake in rat.
Evidence that neurotensin mediates the central effect of leptin on food intake in rat.
复制标题
神经降压素介导瘦素对大鼠食物摄入的中枢作用的证据。
DOI:
10.1016/s0006-8993(00)03107-3
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发表时间:
2001
期刊:
影响因子:
2.9
通讯作者:
Wang,YP
中科院分区:
文献类型:
--
作者:
Sahu,A;Carraway,RE;Wang,YP
Recent evidence suggests that leptin’s action on food intake and body weight regulation is mediated by a number of orexigenic and anorectic neuronal systems in the hypothalamus. Our previous demonstration that central injections of leptin induce hypothalamic neurotensin (NT) gene expression in association with a reduced food intake and decreased body weight in rats indicates that NT, an anorectic peptide, is involved in mediating leptin’s action on feeding and body weight regulation. To begin to examine the relative role of NT in this regard we evaluated the effects of NT antiserum (NT-AS) or NT receptor antagonist, SR 48692, on the satiety action of leptin in rats. In the first experiment, 3rd cerebroventricular (i.c.v.) administration of either 1 or 5 μl of NT-AS, 30 min prior to leptin (4 μg) injection, completely blocked the effects of leptin on food deprivation (FD)-induced feeding. In the second experiment, intraperitoneal (i.p.) administration of SR 48692 (40 μg/kg) also completely prevented leptin’s satiety action on FD-induced feeding. These results showing the reversal of leptin’s satiety action by either NT immunoneutralization or NT-receptor antagonism support our hypothesis that NT is involved in mediating leptin’s action on feeding and further suggest that this neuropeptide is a quantitatively important component of the leptin sensitive neural circuitry.