Abstract
Acetate, propionate and butyrate, three of the most common short chain fatty acids (SCFAs), can be produced when some non-digestible carbohydrates enter the large intestine and undergo bacterial fermentation. This study was designed to investigate the effects of these three SCFAs on appetite regulation and lipid metabolism, and to what extent appetite contributed to the beneficial influences of SCFAs. In a 35-day study, a total of 48 C57BL/6 male mice were randomly allocated into six groups : (1) control; (2) 5% sodium acetate; (3) 5% sodium propionate; (4) 5% sodium butyrate; (5) pair fed 1; (6) pair fed 2. The results showed that sodium acetate reduced serum triglyceride, free fatty acids, glucose and interleukin (IL) 6 levels (P < 0.05), increased serum glucagon-like peptide 1 and leptin levels (P < 0.05), down-regulated the mRNA expressions of fatty acid synthase, peroxisome proliferator activated receptor and lipoprotein lipase (P < 0.05), and up-regulated the mRNA expressions of fasting induced adipose factor, nuclear respiratory factor 1, mitochondrial transcription factor A, tumor necrosis factor receptor superfamily member 9, cytochromec oxidase IV and free fatty acid receptor 2 (P < 0.05). Sodium propionate also reduced serum IL-1β level (P < 0.05), increased serum peptide YY level (P < 0.05), down-regulated the mRNA expressions of acetyl-CoA carboxylase and sterol regulatory element binding protein 1c (P < 0.05), and up-regulated the mRNA expression of transmembrane protein 26 (P < 0.05). Besides, Sodium butyrate decreased average daily feed intake (P < 0.05), down-regulated the mRNA expression of myosin heavy-chain (MyHc) Ⅱb (P < 0.05), and up-regulated the mRNA expressions of lipase hormone-sensitive, MyHC Ⅱa and carnitine palmitoyltransferase-1α (P < 0.05). Moreover, the metabolic benefits of SCFAs were partly attributed to the reduction of feed intake. Taken together, SCFAs could reduce appetite and fat accumulation via modulating relevant genes and hormones, which might further illustrate the potential mechanisms that underlay the impacts of SCFAs on lipid homeostasis and body weight control.