Department of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Tokyo, 183-8509, Japan.
AMED-CREST, Japan Agency for Medical Research and Development, Chiyoda-ku, Tokyo, 100-0004, Japan.
Sci Rep. 2019 Nov 12;9(1):16574. doi: 10.1038/s41598-019-53242-x.
Fermented foods represent a significant portion of human diets with several beneficial effects. Foods produced by bacterial fermentation are enriched in short-chain fatty acids (SCFAs), which are functional products of dietary fibers via gut microbial fermentation. In addition to energy sources, SCFAs also act as signaling molecules via G-protein coupled receptors such as FFAR2 and FFAR3. Hence, dietary SCFAs in fermented foods may have a direct influence on metabolic functions. However, the detailed mechanism by dietary SCFAs remains unclear. Here, we show that dietary SCFAs protected against high-fat diet-induced obesity in mice in parallel with increased plasma SCFAs without changing cecal SCFA or gut microbial composition. Dietary SCFAs suppressed hepatic weight and lipid synthesis. These effects were abolished in FFAR3-deficient mice but not FFAR2-deficient. Thus, SCFAs supplementation improved hepatic metabolic functions via FFAR3 without influencing intestinal environment. These findings could help to promote the development of functional foods using SCFAs.
发酵食品是人类饮食的重要组成部分，具有多种有益作用。细菌发酵产生的食品富含短链脂肪酸 (SCFA)，这些脂肪酸是膳食纤维通过肠道微生物发酵产生的功能性产物。除了作为能量来源外，SCFAs 还通过 G 蛋白偶联受体（如 FFAR2 和 FFAR3）发挥信号分子的作用。因此，发酵食品中的饮食 SCFAs 可能直接影响代谢功能。然而，饮食 SCFAs 的详细机制尚不清楚。在这里，我们表明饮食 SCFAs 通过增加血浆 SCFAs 而不改变盲肠 SCFA 或肠道微生物组成，与高脂肪饮食诱导的肥胖症呈平行关系。饮食 SCFAs 抑制了肝脏重量和脂质合成。这些作用在 FFAR3 缺陷型小鼠中被消除，但在 FFAR2 缺陷型小鼠中没有。因此，SCFAs 补充通过 FFAR3 改善了肝脏代谢功能，而不影响肠道环境。这些发现有助于促进使用 SCFAs 的功能性食品的开发。
