Format

Send to

Choose Destination
Neural Regen Res. 2013 Sep 5;8(25):2379-88. doi: 10.3969/j.issn.1673-5374.2013.25.009.

Metformin inhibits food intake and neuropeptide Y gene expression in the hypothalamus.

Author information

1
Key Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, East China Normal University, Shanghai 200062, China.
2
Department of Clinical Laboratory, Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai 201508, China.

Abstract

Metformin may reduce food intake and body weight, but the anorexigenic effects of metformin are still poorly understood. In this study, Sprague-Dawley rats were administered a single intracere-broventricular dose of metformin and compound C, in a broader attempt to investigate the regula-tory effects of metformin on food intake and to explore the possible mechanism. Results showed that central administration of metformin significantly reduced food intake and body weight gain, par-ticularly after 4 hours. A reduction of neuropeptide Y expression and induction of AMP-activated protein kinase phosphorylation in the hypothalamus were also observed 4 hours after metformin administration, which could be reversed by compound C, a commonly-used antagonist of AMP-activated protein kinase. Furthermore, metformin also improved lipid metabolism by reducing plasma low-density lipoprotein. Our findings suggest that under normal physiological conditions, central regulation of appetite by metformin is related to a decrease in neuropeptide Y gene expres-sion, and that the activation of AMP-activated protein kinase may simply be a response to the anorexigenic effect of metformin.

KEYWORDS:

AMP-activated protein kinase; body weight gain; food intake; grants-supported paper; hypothalamus; metformin; neural regeneration; neuropeptide Y; neuroregeneration

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center