Obesity is a global epidemic and responsible for the development of numerous chronic diseases including type II diabetes mellitus and cardiovascular disease. It is well established that obesity negatively alters circulating and tissue resident immune cell frequencies and functions. Mucosal associated invariant T (MAIT) cells are a population of innate T cells, which express an invariant T cell receptor, restricted by the MHC like molecule MR1. Upon activation MAIT cells can produce several cytokines including IFN-g, TNF-a and IL-17. We have previously reported that MAIT cells are dysregulated in obesity, with altered circulating and adipose tissue frequencies and a reduction in IFN-g production. The mechanisms driving their defective cytokine production are currently unknown. We performed RNA sequencing of MAIT cells isolated from obese adults and reveal extensive alterations in metabolic pathways compared to lean controls. Upon activation, immune cells undergo metabolic reprogramming, this allows for the increased demand for energy and biological intermediates required for the formation of effector proteins such as cytokines. Metabolic reprogramming can also determine the type of immune response elicited by specific immune cells. The metabolic pathways utilized by MAIT cells are currently unknown. In this report, we demonstrate that both cellular glycolysis and oxidative phosphorylation are important for MAIT cell cytokine production. We show that obesity induces defects in glucose consumption, mTOR activation and glycolytic metabolism, which explains the loss of IFN-g production previously reported in obesity.  Collectively our data shows the intrinsic metabolic pathways controlling MAIT cell cytokine production and highlight a mechanism for the altered MAIT cell responses reported in obesity.