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Several histone deacetylase (HDAC) inhibitors have been shown to play beneficial roles in treating obesity and its related metabolic syndromes. However, the underlying mechanisms are still not understood well. In this study, we examined the potential roles of SAHA, a potent inhibitor of HDACs, on energy expenditure and explored the molecular mechanism involved. Our data showed that SAHA induces less lipid accumulation and smaller lipid droplets in cultured adipocytes.  In vivo  studies showing SAHA reduces body weight gain and increases core temperature in lean and obese mice. Furthermore, SAHA accelerates blood glucose disposal, improves insulin sensitivity and attenuates fatty liver in obese animals. Transcriptome sequencing found that a group of zinc finger proteins ( Zfps ) was up-regulated by SAHA. Functional studies showed that the knockdown of  Zfp691  or  Zfp719  largely abolishes SAHA-induced  Ucp1  expression in adipocytes. ChIP assay showed that SAHA stimulates histone H3 acetylation at  Zfp719  promoter. Luciferase reporter analysis revealed that  Zfp719  activates  Ucp1  promoter. As a consequence, forced expression of  Zfp719  increases  Ucp1  expression and promotes lipid catabolism in adipocytes. Taken together, our data indicate that by stimulating axis of ZFPs-UCP1, SAHA induces white fat browning and energy consumption, which makes it a potential drug for treating obesity and related metabolic dysfunctions.

SAHA induces white fat browning and rectifies metabolic dysfunctions via activation of ZFPs