Acute oral sodium propionate supplementation raises resting energy expenditure and lipid oxidation in fasted humans

Abstract

Short-chain fatty acids (SCFAs), produced from fermentation of dietary fibre by the gut microbiota, have been suggested to modulate energy metabolism. Previous work using rodent models has demonstrated that oral supplementation of the SCFA propionate raises resting energy expenditure (REE) by promoting lipid oxidation. The objective of the present study was to investigate the effects of oral sodium propionate on REE and substrate metabolism in humans. Eighteen healthy volunteers (9 women and 9 men; age 25 ± 1 years; body mass index 24.1 ± 1.2 kg/m² ) completed 2 study visits following an overnight fast. Tablets containing a total of 6845 mg sodium propionate or 4164 mg sodium chloride were provided over the 180-minute study period in random order. REE and substrate oxidation were assessed by indirect calorimetry. Oral sodium propionate administration increased REE (0.045 ± 0.020 kcal/min; P = .036); this was accompanied by elevated rates of whole-body lipid oxidation (0.012 ± 0.006 g/min; P = .048) and was independent of changes in glucose and insulin concentrations. Future studies are warranted to determine whether the acute effects of oral sodium propionate on REE translate into positive improvements in long-term energy balance in humans.

Keywords: dietary intervention; energy regulation; randomized trial.

Figure 1

The effect of oral sodium propionate supplementation on short chain fatty acid levels in peripheral blood. A, Propionate (time × trial P = .043) and B, Propionate incremental area under the curve (iAUC; P = .021). C, Acetate (time × trial P = .209) and D, Acetate iAUC (P = .761). E, Butyrate (time × trial P = .272) and F, Butyrate iAUC (P = .587). All data expressed as mean ± SEM (n = 18)

Figure 2

Effect of oral sodium propionate supplementation on resting energy expenditure and substrate oxidation. A, Resting energy expenditure (REE; time × trial P = .388) and B, REE incremental area under the curve (iAUC; P = .036). C, Respiratory exchange ratio (RER; time × trial P = .158) and D, Mean RER (P = .040). E, Lipid oxidation (time × trial P = .075) and F, Lipid oxidation iAUC (P = .019). G, Carbohydrate oxidation (time × trial P = .199) and H, Carbohydrate oxidation iAUC (P = .338). All data expressed as mean ± SEM (n = 18)