Abstract
Background and Objectives:The gut hormones peptide YY (PYY) and glucagon-like peptide 1 (GLP-1) acutely suppress appetite. The short chain fatty acid (SCFA) receptor, free fatty acid receptor 2 (FFA2) is present on colonic enteroendocrine L cells, and a role has been suggested for SCFAs in appetite regulation. Here, we characterise the in vitro and in vivo effects of colonic propionate on PYY and GLP-1 release in rodents, and investigate the role of FFA2 in mediating these effects using FFA2 knockout mice.Methods:We used Wistar rats, C57BL6 mice and free fatty acid receptor 2 knockout (FFA−/−) mice on a C57BL6 background to explore the impact of the SCFA propionate on PYY and GLP-1 release. Isolated colonic crypt cultures were used to assess the effects of propionate on gut hormone release in vitro. We subsequently developed an in vivo technique to assess gut hormone release into the portal vein following colonic infusion of propionate.Results:Propionate stimulated the secretion of both PYY and GLP-1 from wild-type primary murine colonic crypt cultures. This effect was significantly attenuated in cultures from FFA2−/− mice. Intra-colonic infusion of propionate elevated PYY and GLP-1 levels in jugular vein plasma in rats and in portal vein plasma in both rats and mice. However, propionate did not significantly stimulate gut hormone release in FFA2−/− mice.Conclusions:Intra-colonic administration of propionate stimulates the concurrent release of both GLP-1 and PYY in rats and mice. These data demonstrate that FFA2 deficiency impairs SCFA-induced gut hormone secretion both in vitro and in vivo.
Highlights
The anorexigenic gut hormone peptide YY (PYY) and the incretin glucagon-like peptide 1 (GLP-1) acutely suppress appetite following their co-release from enteroendocrine L cells.[1]
Evidence suggests that the displacement of nutrients in the gut caused by procedures such as the RYGB may mediate the dramatic effects on weight loss and type 2 diabetes of these surgeries, at least in part through the release of PYY and GLP-1.2,3 An understanding of how nutrients stimulate PYY and GLP-1 secretion could lead to more effective nutritional management and/or prevention of obesity
Our studies demonstrate that intra-colonic administration of propionate stimulates the concurrent release of both GLP-1 and PYY in rodents, and demonstrate in vitro, and for the first time in vivo, that free fatty acid receptor 2 (FFA2) deficiency impairs short chain fatty acid (SCFA)-induced gut hormone secretion
Summary
The anorexigenic gut hormone peptide YY (PYY) and the incretin glucagon-like peptide 1 (GLP-1) acutely suppress appetite following their co-release from enteroendocrine L cells.[1]. Isolated colonic crypt cultures were used to assess the effects of propionate on gut hormone release in vitro. We subsequently developed an in vivo technique to assess gut hormone release into the portal vein following colonic infusion of propionate. RESULTS: Propionate stimulated the secretion of both PYY and GLP-1 from wild-type primary murine colonic crypt cultures. This effect was significantly attenuated in cultures from FFA2− / − mice. CONCLUSIONS: Intra-colonic administration of propionate stimulates the concurrent release of both GLP-1 and PYY in rats and mice. These data demonstrate that FFA2 deficiency impairs SCFA-induced gut hormone secretion both in vitro and in vivo
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