Zinc-α2-Glycoprotein Knockout Influenced Genes Expression Profile in Adipose Tissue and Decreased the Lipid Mobilizing After Dexamethasone Treatment in Mice

Zinc-α2-glycoprotein (ZAG), as an adipokine, plays an important role inlipid metabolism. However, its influence on whole gene expression profile inadipose tissue is not known. Under stress condition, how ZAG affects the lipidmetabolism is also unclear. Therefore, in this study ZAG systemic knockout (KO)mice were used as a model to reveal the genes expression profile in visceral fattissues of ZAG KO mice and wild-type mice by genome-wide microarray screening.Then dexamethasone (DEX) was used to explore the effect of ZAG deletion on bodyfat metabolism under stress. Our results showed that 179 genes weredifferentially expressed more than 1.5 times between ZAG KO mice and wild typemice, of which 26 genes were upregulated dramatically and 153 genes weresignificantly downregulated. Under DEX simulated stress, ZAG systemic knockoutin vivo resulted in a markedly decrease of triglycerides (TG) and nonesterifiedfatty acid (NEFA) content in in plasma. Similarly, for lipid catabolism, ZAG KOled to a significant increase of phosphorylated HSL (p-HSL) protein and a risingtendency of adipose triglyceride lipase (ATGL) protein relative to those of theDEX group. For lipid anabolism, fatty acid synthase (FAS) and adiponectinprotein expression in visceral fat rose notably in ZAG KO mice after DEXtreatment. In conclusion, ZAG knockout can affect the gene expression profile ofadipose tissue, reduce elevated TG and NEFA levels in plasma, and alter lipidmetabolism under DEX treatment. These findings provide new insights into themechanism of lipid metabolic disorders in response to stress.