Department of Medicine: Student Research and Presentations
ADIPOSE HDAC9 DELETION PROTECT AGAINST DIET INDUCED OBESITY IN MICE THROUGH REGULATING ENERGY EXPENDITUREOur group has previously identified histone deacetylase 9 (HDAC9) as a regulator of adipocyte differentiation, and its expression levels were elevated in diet induced obese (DIO) mice.� We also reported that global HDAC9 deletion protected mice against DIO through promoting beige adipogenesis. Here, we hypothesized that adipose HDAC9 correlate with human obesity similar to murine models, and its deletion is sufficient to protect against DIO. To test this hypothesis we crossed HDAC9 floxed mice with adiponectin-cre mice to generate adipose-specific HDAC9 knockout mice (AdipCre-HDAC9), which exhibited 30% less weight gain when fed high fat diet compared to control despite increased food intake, in association with increased energy combustion & O2 consumption, improved insulin sensitivity and glucose tolerance. However, unlike global HDAC9 deletion, this was not associated with increased beige adipogenesis nor increase in brown adipose tissue function. Interestingly, AdipoCre-HDAC9 mice fed normal chow diet didn�t exhibit altered energy expenditure nor weight differences when compared to littermate controls. These finding suggest that adipose HDAC9 regulate energy expenditure in response to high fat diet and can be a promising therapeutic target to combat obesity.