Bifidobacterium animalis subsp. lactis A6 Enhances Fatty Acid β-Oxidation of Adipose Tissue to Ameliorate the Development of Obesity in Mice

Abstract

Fatty acid β-oxidation (FAO) is confirmed to be impaired in obesity, especially in adipose tissues. We previously proved that Bifidobacterium animalis subsp. lactis A6 (BAA6) had protective effects against diet-induced obesity. However, whether BAA6 enhances FAO to ameliorate the development of obesity has not been explored. After being fed with high-fat diet (HFD) for 9 weeks, male C57BL/6J mice were fed HFD or BAA6 for 8 weeks. In vitro study was carried out using 3T3-L1 adipocytes to determine the effect of BAA6 culture supernatant (BAA6-CM). Here, we showed that administration of BAA6 to mice fed with HFD decreased body weight gain (by 5.03 g) and significantly up-regulated FAO in epididymal adipose tissues. In parallel, FAO in 3T3-L1 cells was increased after BAA6-CM treatment. Acetate was identified as a constituent of BAA6-CM that showed a similar effect to BAA6-CM. Furthermore, acetate treatment activated the GPR43-PPARα signaling, thereby promoting FAO in 3T3-L1 cells. The levels of acetate were also elevated in serum and feces (by 1.92- and 2.27-fold) of HFD-fed mice following BAA6 administration. The expression levels of GPR43 and PPARα were increased by 55.45% and 69.84% after BAA6 supplement in the epididymal fat of mice. Together, these data reveal that BAA6 promotes FAO of adipose tissues through the GPR43-PPARα signaling, mainly by increasing acetate levels, leading to alleviating the development of obesity.

Gestational supplementation of Bifidobacterium, Lactobacillus, and Streptococcus thermophilus attenuates hepatic steatosis in offspring mice through promoting fatty acid β‐oxidation

“…Previous studies have shown that maternal L. reuteri supplementation alleviated placental oxidative damage induced by maternal HFD and had a positive effect on hepatic steatosis in fetus, which is achieved by recoding key enzymes related to lipid metabolism (Yu et al., 2022). In several other animal studies, it was found that the β‐oxidation in the liver or epididymal adipose tissues of mice was activated by probiotic intervention (Huo et al., 2022; Park et al., 2013; Yoon et al., 2023). In these above studies, PPARα was up‐regulated to varying degrees after probiotic intervention.…”

New Insights into High-Fat Diet with Chronic Diseases

“…Meanwhile, Y. Huo et al found that Bifidobacterium animalis subsp. lactis A6 enhances adipose tissue fatty acid β-oxidation (FAO) to mitigate obesity development by increasing acetate levels and activating the GPR43-PPARα signaling pathway in mice [ 5 ].…”

Modulation of adipose tissue metabolism by microbial-derived metabolites

“…Previous studies have shown that all three major SCFAs can promote lipogenic differentiation of 3 T3-L1 pre-adipocytes. Acetate treatment of 3 T3-L1 pre-adipocytes leads to an increase in the expression of genes related to lipogenic differentiation (Huo et al, 2022). Hong et al showed upregulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) and GPR43 mRNA expression in 3 T3-L1 cells treated with acetate or propionic acid for 7 days; this effect was counteracted in the absence of GPR43 (Hong et al, 2005).…”