Diabetes is a chronic disease that affects millions of people and will affect millions more in the coming generation. Symptoms of type 2 diabetes (T2D) include weight gain, impaired glucose tolerance, and impaired insulin secretion. Nuclear receptor Nr4a3 controls gene expression of targets essential for fuel metabolism and respiration. In patients with type 2 diabetes Nr4a3 promoter is hypermethylated, and Nr4a3 expression is downregulated. I sought to understand the effect of systemic Nr4a3 loss. Mice with knockout (KO) nuclear receptor Nr4a3 manifest symptoms of T2D including impaired glucose tolerance, impaired insulin secretion and increased adiposity. Nr4a3 plays a crucial role in controlling adipose mitochondrial respiration. Elucidating the role of Nr4a3 in mitochondrial respiration in adipose will help define the mechanism of T2D onset and treatment. Full body Nr4a3 KO animals were fed a standard diet. Male animals demonstrated impaired glucose and insulin tolerance. I measured mitochondrial respiration in muscle, liver, kidney, and adipose tissue, with impaired respiration only observed in adipose tissue. The impaired adipose respiration corresponds with increased mass of all adipose depots, increased adipocyte size, and increased lipid droplet size. Given the observed adipose respiration, I hypothesized that the impaired respiration is due to decreased expression of ETC components or TCA cycle dehydrogenases that fuel the ETC. These results and the implications on T2D will be presented in the upcoming UCUR conference.