Regulation Of GPR120 On Lipid Metabolism And Inflammatory Responses In Bovine Adipocytes

Transition cows generally have different degrees of negative energy balance.Negative energy balance causes fat mobilization in bovine adipose tissue.Massive lipolysis causes a large amount of free fatty acids(FFA)produced in the body to cause metabolic disorders such as ketosis and fatty liver with systemic inflammatory responses.The occurrence of vegetative metabolic disorders such as ketosis often has a mass-generating effect,which increases the risk of dairy cows suffering from other diseases while causing a decrease in the milk yield of dairy cows and causes huge economic losses to the dairy farming industry in China.Therefore,prevention and treatment of ketosis in perinatal dairy cows is one of the urgent problems to be solved in China’s dairy farming industry.G protein-coupled receptor 120(GPR120)is expressed as a membrane protein receptor in various tissues of animals.Studies in humans and mice have shown that GPR120 is abundantly expressed in the human small intestine and is predicted to participate in the body’s digestive process;GPR120 is also abundantly expressed in adipose tissue of mice,suggesting that it may be involved in the proliferation and differentiation of adipocytes.However,little is known about GPR120 in bovine adipocytes.In this study,gene interference technology was used to study the regulation of GPR120 on bovine adipocytes by silencing GPR120 in primary cultured bovine adipocytes and GPR120 was activated by GPR120 agonist TUG-891.The results showed that the content of peroxisome proliferators-activated receptor gamma 2(PPARγ2),sterol regulatory element binding protein 1c(SREBP-1c),and lipid droplet coating protein(PLIN1)were silenced in the GPR120 group;fatty acid synthase(FAS),diacylglycerol acyltransferase 1(DGAT1)and triglyceride(TG)were decreased significantly when compared with the blank control group.However,activation of GPR120 reduced the expression of PPARγ2,SREBP-1c,PLIN1,FAS,TG while reducing the expression of hormone-sensitive lipase(HSL)gene.The addition of lipopolysaccharide(LPS)to bovine adipocytes induces cellular inflammatory responses and silences GPR120 and activates GPR120,respectively.The results showed that compared with the control group,p65,interleukin-6(IL-6),interleukin-1β(IL-1β),interleukin-18(IL-18),and NLRP3 were observed in the adipocytes of the GPR120-silencing group.The expression level was significantly increased;while activation of GPR120 significantly inhibited the expression of p65,IL-6,IL-1β,IL-18,and NLRP3.The above results indicate that GPR120 can promote the lipid synthesis of bovine adipocytes in dairy cows and alleviate the inflammatory response of induced by LPS.This study provides a new theoretical basis and data support for the clinical prevention and treatment of ketosis.