کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1929841 | 1050476 | 2012 | 6 صفحه PDF | دانلود رایگان |

Glucagon-like peptide-1 (GLP-1) and leptin are anorectic hormones produced in the small intestine and white adipose tissue, respectively. Investigating how these hormones act together as an integrated anorectic signal is important to elucidate a mechanism to maintain energy balance. In the present study, coadministration of subthreshold GLP-1 and leptin dramatically reduced feeding in rats. Although coadministration of GLP-1 with leptin did not enhance leptin signal transduction in the hypothalamus, it significantly decreased phosphorylation of AMP-activated protein kinase (AMPK). In addition, coadministration of GLP-1 with leptin significantly increased proopiomelanocortin (POMC) mRNA levels. Considering that α-melanocortin stimulating hormone (α-MSH) is derived from POMC and functions through the melanocortin-4-receptor (MC4-R) as a key molecule involved in feeding reduction, the interaction of GLP-1 and leptin on feeding reduction may be mediated through the α-MSH/MC4-R system. As expected, the interaction of GLP-1 and leptin was abolished by intracerebroventricular preadministration of the MC4-R antagonists agouti-related peptide and SHU9119. Taken together, GLP-1 and leptin cooperatively reduce feeding at least in part via inhibition of AMPK following binding of α-MSH to MC4-R.
► We investigate the interaction of GLP-1 and leptin on feeding.
► Coinjection of subthreshold of these two hormones significantly decreases feeding.
► Coinjection of these two hormones dramatically decreases AMPK in the hypothalamus.
► Coinjection of these two hormones significantly increases POMC mRNA.
► Blockade of POMC/MC4-R cancels feeding reduction induced by GLP-1 + leptin.
Journal: Biochemical and Biophysical Research Communications - Volume 420, Issue 1, 30 March 2012, Pages 36–41