Topical Area: Obesity, Energy and Macronutrient Metabolism
Fermentation of fiber in the gut generates short-chain fatty acids (SCFA), such as butyrate, which decrease food intake and promote weight loss in rodent models. SCFA have been shown to enhance secretion of the gut satiety hormone peptide YY (PYY). However, it is unknown whether PYY is causative to SCFA-induced changes in energy balance. Our objectives were to determine the dose-response effects of butyrate on energy balance, and assess whether PYY signaling is essential for mediating the satiety effects of butyrate.
Male Sprague Dawley rats (8 wks old, n=39) were randomized to one of three isocaloric (4.63 kcal/g) diets: 1) control (0% sodium butyrate, n=14), 2) 5% sodium butyrate (n=13), or 3) 10% sodium butyrate (n=12), and followed for upto 4 weeks. A PYY Y-2 receptor antagonist (BIIE0246) or vehicle were administered IP acutely during the study. Measurements included food intake, respiratory quotient, and energy expenditure (CLAMS®), and body composition (Minispec LF110 NMR).
Compared to control, 10% sodium butyrate decreased food intake and respiratory quotient for 4 days, whereas, 5% sodium butyrate was ineffective. Notably, compared to control, 10% sodium butyrate decreased body weight and fat gain without changing energy expenditure. Importantly, systemic Y-2 receptor blockade stimulated food intake and increased respiratory quotient, without altering energy expenditure, only in 10% sodium butyrate group.
We found that dietary butyrate dose-dependently decreases food intake and respiratory quotient. Importantly, Y-2 receptor blockade attenuated butyrate-induced hypophagia, which supports a role for endogenous PYY in the satiety effects of dietary butyrate.
Funding Sources : NSERC, Heart and Stroke Foundation of Canada.