AIM To investigate the effects of nesfatin-1 on gastric function in obese rats. METHODS The obese rat model was induced by a high-fat diet. The gastric emptying rate and gastric acid secretory capacity of the rats wer...AIM To investigate the effects of nesfatin-1 on gastric function in obese rats. METHODS 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. RESULTS Body weight, body length, and Lee's index of the rats significantly increased in the high-fat dietinduced 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. Thisin 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.CONCLUSION Through this research, we provide a theoretical basis for further studies on nesfatin-1, a potential antiobesity drug.展开更多
基金Supported by Cangzhou City Science and Technology Plan Projects,No.151302138
文摘AIM To investigate the effects of nesfatin-1 on gastric function in obese rats. METHODS 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. RESULTS Body weight, body length, and Lee's index of the rats significantly increased in the high-fat dietinduced 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. Thisin 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.CONCLUSION Through this research, we provide a theoretical basis for further studies on nesfatin-1, a potential antiobesity drug.
