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本研究采用GLP-1阻滞剂进行研究，结果发现该物质可以减弱瘦素对于食欲的抑制。证实内源性的GLP-1可以影响瘦素（leptin）对于摄食中枢的调节。

Leptin and glucagon-like peptide-1 (GLP-1) were proved to act in concert to control the activity of feeding centres. Since leptin receptor was identified in the gut endocrine L cells and neurons producing GLP-1, we have checked whether GLP-1 mediates the effects of leptin on feeding and drinking behaviour.

To this aim, an intraperitoneal or intracerebroventricular injection of exendin (9 - 39), a GLP-1 antagonist, (50 or 10 µg per rat, respectively) followed by leptin (100 or 5 µg per rat, respectively) was made and 24-hour food intake and body weight changes were measured. Previous injection of exendin (9 - 39) completely abolished the suppressory effect of peripheral leptin on food intake and body weight gain. Moreover, exendin (9 - 39) significantly attenuated the effect of intracerebroventricular leptin on food but not water consumption.

It is concluded that intact GLP-1 signalling is necessary to mediate the effect of leptin on food intake in the rat. Conversely, leptin seems to affect the thirst center function independently of GLP-1. Also, these findings produce further evidence for close interactions between long- and short-term factors regulating the activity of feeding centres.