Lactobacillus rhamnosus Hsryfm 1301 Fermented Milk Regulates Lipid Metabolism and Inflammatory Response in High-Fat Diet Rats

Abstract

A rat model of disordered lipid metabolism was established to study the regulation of lipid metabolism and inflammatory response by Lactobacillus rhamnosus hsryfm 1301 fermented milk. The results showed that the high-fat diet caused the disorder of lipid metabolism in rats, accompanied by the occurrence of an inflammatory response. After Lactobacillus rhamnosus hsryfm 1301 fermented milk intervention, the blood lipid level was reduced along with the activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as well as triglyceride (TG) and total cholesterol (TC) contents in the liver of rats (p < 0.05), the fat vacuoles of rat hepatocytes were reduced, and the lipid accumulation in the rat liver was decreased. Liver injury was restored. Meanwhile, the levels of free fatty acid (FFA) and fatty acid synthase (FAS), acetyl coenzyme A carboxylase (ACC), lipoprotein esterase (LPL) and hepatic lipase (HL) in serum and liver of rats were significantly lower than those in the model group (p < 0.05), which indicated that fatty acid synthesis was inhibited, fatty acid production was reduced and lipid metabolism was restored to balance. In addition, the levels of reactive oxygen species (ROS) and inflammatory factors in the serum of rats were also significantly reduced (p < 0.05), and the inflammatory response of rats was restored. Lactobacillus rhamnosus hsryfm 1301 fermented milk could not only inhibit fatty acid synthase but reduce the production of excessive fatty acids, thus reducing fat accumulation, restoring the balance of lipid metabolism and alleviating the inflammatory response in rats. At the same time, it can also reduce the level of ROS through the antioxidant effect, alleviate the inflammatory response, and thus alleviate the disorder of lipid metabolism.

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“…LPL and HL are key enzymes in lipolysis and are important lipases for TG catabolism ( 48 ). The reduction in the activity of LPL and HL is thought to be a side effect of the restoration of lipid metabolic homeostasis, which in turn further normalizes lipolysis ( 49 ).…”