Hypothalamic CART is a new anorectic peptide regulated by leptin
Hypothalamic CART is a new anorectic peptide regulated by leptin
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DOI：
10.1038/29993
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发表时间：
1998-05-07
期刊：
影响因子：
64.8
通讯作者：
Hastrup, S
中科院分区：
文献类型：
--
作者：
Kristensen, P;Judge, ME;Hastrup, S
哺乳动物的下丘脑通过几个不同的信号分子和受体系统强烈影响摄食行为(1-4)。在这里，我们发现CART(可卡因和苯丙胺调节的转录本)，一个大脑定位的多肽(5-8)，是一个饱足因子，并与两个重要的食物摄取调节因子瘦素和神经肽Y的作用密切相关。食物剥夺动物显示出CART信使RNA在弓状核中的表达显著减少。在瘦素信号中断的肥胖动物模型中，CART mRNA几乎不存在于弓状核。肥胖小鼠外周应用瘦素可刺激CART基因表达。将重组CART多肽注入大鼠侧脑室，可抑制正常摄食和饥饿诱导的摄食，并完全阻断神经肽Y诱导的摄食反应。CART抗血清可增加正常大鼠的摄食，提示CART可能是正常动物摄食的内源性抑制因子。
The mammalian hypothalamus strongly influences ingestive behaviour through several different signalling molecules and receptor systems(1-4). Here we show that CART (cocaine-and amphetamine-regulated transcript), a brain-located peptide(5-8), is a satiety factor and is closely associated with the actions of two important regulators of food intake, leptin and neuropeptide Y. Food-deprived animals show a pronounced decrease in expression of CART messenger RNA in the arcuate nucleus. In animal models of obesity with disrupted leptin signalling, CART mRNA is almost absent from the arcuate nucleus. Peripheral administration of leptin to obese mice stimulates CART mRNA expression. When injected intracerebroventricularly into rats, recombinant CART peptide inhibits both normal and starvation-induced feeding, and completely blocks the feeding response induced by neuropeptide Y. An antiserum against CART increases feeding in normal rats, indicating that CART may be an endogenous inhibitor of food intake in normal animals.