Derangement of ghrelin secretion after long‐term high‐fat diet feeding in rats

Abstract

Aim: Appetite control is an important goal for the management of non-alcoholic fatty liver disease, diabetes mellitus and obesity; however, little is known about how hormones concerning appetite regulation are affected by long-term consumption of a high-fat diet. We investigated the effect of high-fat diet on secretory regulation of ghrelin and leptin in rats.Methods: Rats were fed a control or a high-fat diet for 18 weeks and then killed. Before being killed, a glucose tolerance test was performed. Weight, total calorie intake and blood glucose levels were measured, and the plasma levels of total and active ghrelin, and leptin were analyzed by enzyme-linked immunosorbent assay.Results: Body and fat weight and total calorie intake were significantly higher in the high-fat diet group than in the control, although blood glucose levels did not differ. Plasma leptin was significantly higher in the high-fat diet group, and a significant positive correlation was observed between bodyweight and leptin levels in both groups. The levels of active and total ghrelin were not significantly changed by high-fat diet, and active ghrelin levels in the control group significantly correlated negatively with bodyweight, while its correlation was lost in the high-fat diet group. The glucose tolerance test showed that ghrelin levels were significantly higher than those of controls even 60 min after glucose loading. Conclusion:These results indicate that secretion of ghrelin, but not leptin, are deranged by consumption of a high-fat diet, and active ghrelin levels lose their correlation with bodyweight and food intake.

Voluntary exercise contributed to an amelioration of abnormal feeding behavior, locomotor activity and ghrelin production concomitantly with a weight reduction in high fat diet-induced obese rats

“…The induction of periodic voluntary exercise ameliorated the disrupted ghrelin production to nearly the control levels, with a concomitant decrease in body weight and fat, in line with the results of a human study [15], but conflicting with the results in other reports [16,17]. Considering these results with the deranged ghrelin production in HFD-obese rats [34], possible explanations for the inconsistencies among studies are as follows. The degrees of obesity may have been different among studies, ranging from mild to genetically deficient severe obesity.…”

Silencing of microRNA‐122 is an early event during hepatocarcinogenesis from non‐alcoholic steatohepatitis

“…Tissue samples and blood were obtained from both control and STAM mice. Histological and biochemical examinations were carried out as described previously . All animals had free access to water and food and were maintained in a temperature‐controlled specific pathogen‐free animal facility.…”

“…Histological and biochemical examinations were carried out as described previously. (16) All animals had free access to water and food and were maintained in a temperature-controlled specific pathogen-free animal facility. All experiments and procedures were approved by the Keio University Animal Research Committee.…”

The modulatory role of high fat feeding on gastrointestinal signals in obesity

“…Centrally, GHSR levels are decreased in the hypothalamus, and NPY/AgRP neuronal signaling is diminished [134]. This compensation is also seen peripherally, as most studies demonstrate a decrease in circulating ghrelin levels of HF fed obese animals [135][136][137][138][139]202], although this is not always the case [221]. For example, in Long-Evans rats fed a HF diet, plasma ghrelin was decreased almost 25% compared to rats fed a control diet with a strong negative correlation between fat intake and ghrelin levels, although there was a similar correlation between fat pad weight and ghrelin levels [135].…”