Published online Apr 28, 2017. doi: 10.3748/wjg.v23.i16.2940
Peer-review started: December 2, 2016
First decision: December 28, 2016
Revised: February 15, 2017
Accepted: March 2, 2017
Article in press: March 2, 2017
Published online: April 28, 2017
Processing time: 147 Days and 14.5 Hours
To investigate the effects of nesfatin-1 on gastric function in obese rats.
The obese rat model was induced by a high-fat diet. The gastric emptying rate and gastric acid secretory capacity of the rats were determined after treatment with different drug concentrations of nesfatin-1 and administration routes. Based on this, the expression of H+/K+-ATPase was measured using RT-PCR and western blot to preliminarily explore the mechanism of gastric acid secretion changes.
Body weight, body length, and Lee’s index of the rats significantly increased in the high-fat diet-induced obese rat model. Two hours after lateral intracerebroventricular injection of nesfatin-1, the gastric emptying rate and gastric acid secretory capacity of rats decreased. Four hours after injection, both were restored to normal levels. In addition, the expression of H+/K+-ATPase decreased and moved in line with changes in gastric acid secretory capacity. This in vivo experiment revealed that intracerebroventricular injection of nesfatin-1, rather than intravenous injection, could suppress gastric function in obese rats. Moreover, its effect on the gastric emptying and gastric acid secretory capacity of rats is dose-dependent within a certain period of time.
Through this research, we provide a theoretical basis for further studies on nesfatin-1, a potential anti-obesity drug.
Core tip: The high-fat diet-induced obese rat model was used to study the effects of nesfatin-1 on gastric function. We found that intracerebroventricular injection of nesfatin-1, rather than intravenous injection, could suppress gastric function in a dose-dependent manner within a certain period of time. In addition, the expression of H+/K+ ATPase was down-regulated, which may explain the mechanisms of gastric acid secretion changes.
