Student Presenter(s): Shang Lee
Faculty Mentor: Maria Alicia Carrillo Sepulveda
School/College: Osteopathic Medicine, Old Westbury

PPARγ plays a role in glucose and lipid metabolism that can be regulated by acetylation causing vasculo-protective role and obesity-related role in metabolic dysregulation. We hypothesized that PPARγ deacetylation prevents obesity-induced glucose and lipid dysregulation in male mice. Eight-week-old male mice with deacetylated PPARγ containing a LYS to ARG mutation (2KR mice) and C57BL/6 mice were randomized into two experimental groups. Control Groups (n=8 C57BL/6; n=5 2KR); standard diet (5% fat) and Western Diet (WD) Groups (n=12 C57BL/6; n=5 2KR); WD (21% fat) for 16 weeks. Body weight was measured weekly and metabolic parameters monthly. Serum triglyceride and total cholesterol were analyzed via blood samples post terminal. Mid-scapular brown adipose tissue (BAT) was collected for histological analysis. Both cohorts developed obesity as confirmed by increased body weight, BMI, and waist circumference. Obese C57BL/6 mice exhibited glucose intolerance, elevated fasting blood glucose levels and cholesterol levels. Obese 2KR male mice did not exhibit changes in fasting blood glucose level but showed elevated cholesterol levels. Also, 2KR obese female mice showed protection against hypercholesterolemia. The analysis of BAT from obese C57BL/6 mice showed larger unilocular droplets while obese 2KR mice maintained the phenotype. Our results show that PPARγ deacetylation protects against metabolic dysregulation caused by obesity despite weight gain.