A 35 amino acid fragment of leptin inhibits feeding in the rat.
A 35 amino acid fragment of leptin inhibits feeding in the rat.
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瘦素的 35 个氨基酸片段抑制大鼠的摄食。
DOI：
10.1210/endo.137.11.8895397
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发表时间：
1996
期刊：
影响因子：
4.8
通讯作者：
J. Chang
中科院分区：
文献类型：
--
作者：
W. Samson;T. Murphy;D. Robison;T. Vargas;E. Tau;J. Chang
测试了较大的167个氨基酸的肥胖基因相关肽（OBGRP）瘦素的肽片段抑制大鼠进食的能力。C-末端片段OBGRP 116-167在侧脑室给药时仅产生极轻微的摄食抑制。OBGRP 57-92给药后未观察到摄食变化。我们假设瘦素的饱腹感效应存在于肽序列的N-末端区域。在35个氨基酸片段OBGRP 22-56的中央给药后，观察到显著的、剂量相关的和可逆的摄食抑制。这些结果表明，一个小的，容易合成的片段的167个氨基酸的肽瘦素可以发挥生理相关的饱腹感的影响，揭示了内分泌反馈机制，脂肪细胞可以调节下丘脑功能。
Peptide fragments of the larger 167 amino acid obesity gene related peptide (OBGRP), leptin, were tested for their ability to inhibit feeding in the rat. The C-terminal fragment, OBGRP 116-167 exerted only minimal inhibition of feeding when administered into the lateral cerebroventricle. No alteration in feeding was observed following administration of OBGRP 57-92. We hypothesized that the satiety effects of leptin reside in the N-terminal region of the peptide sequence. Significant, dose-related, and reversible inhibition of food intake was observed following central administration of the 35 amino acid fragment OBGRP 22-56. These results suggest that a small, readily synthesized fragment of the 167 amino acid peptide leptin may exert physiologically relevant satiety effects in brain revealing an endocrine feedback mechanism by which the adipocyte may modulate hypothalamic function.
影响因子：
56.9
作者：
HALAAS, JL;GAJIWALA, KS;FRIEDMAN, JM
通讯作者：
FRIEDMAN, JM