Abstract:Lactic acid bacteria are a representative probiotic in human intestine that affect host lipid metabolism, which is closely related with the production of bile salt hydrolase (EC3.5.1.24, BSH) and the conjugate conversion of polyunsaturated fatty acids (PUFAs). The production of BSH and conjugated fatty acids is influenced by strain differences, flora distribution, and dietary differences. This paper focuses on the mechanism of BSH and conjugated fatty acids in regulating the host lipid metabolism, in order to provide reference for further research. BSH can degrade bile acids (BAs) secreted by liver and reduce the absorption of lipids. The degradation products of BAs, deoxycholic acid and lithocholic acid, can promote cholesterol transport and conversion to BAs through signaling pathways such as farnesoid X receptor, small heterodimer partner and liver X receptor. Additionally, BSH can also inhibit lipid synthesis and promote lipid decomposition by down-regulating sterol regulatory element binding protein 1c, up-regulating 5ʹ-AMP activated protein kinase and peroxisome proliferator-activated receptor α (PPARα). PUFAs can be converted into conjugated fatty acids by lactic acid bacteria, such as conjugated linoleic acid (CLA) and conjugated linolenic acid (CLNA). CLA/CLNA boosts the production of leptin in the body, suppresses appetite and promotes energy consumption. Moreover, CLA/CLNA can promote the oxidative decomposition of human lipids by activating PPARα. Lactic acid bacteria modulate the host lipid metabolism through the above-mentioned multiple pathways, which is of great significance for the in-depth understanding of its regulatory mechanism and clinical application.
