2460-P: Relationships between Body Composition and Brain Glucose Transport and Metabolism

Introduction and Objective: Previously, our group and others have shown that obesity is associated with impaired brain glucose metabolism. Here, we examine relationships between body composition metrics and brain metabolism to investigate whether increased fat mass is associated with reduced brain glucose transport. Methods: Eighteen healthy adults from a previously published study were included in this analysis. Eleven lean adults (age 26.5 ± 5.6 years, BMI 21.2 ± 1.7 kg/m2, A1c 5.4 ± 0.2%) and seven obese adults (age 28.3 ± 3.9 years, BMI 32.1 ± 1.5 kg/m2, A1c 5.3 ± 0.4%) underwent 13C magnetic resonance spectroscopy (MRS) scanning paired with a with [1-13C] glucose infusion to measure brain glucose uptake. Participant body composition measurements including fat mass, fat percent, and fat free mass (FFM) were quantified utilizing a bioelectrical impedance scale (Tanita). Results: Individuals with obesity had greater FFM (p = 0.008) as well as fat mass (p <0.0001) compared to lean. In contrast to our hypothesis, there were no significant relationships between fat mass and brain glucose (r=0.4, p=0.15) as well as fat % and brain glucose (r=0.18, p=0.52). Instead, significant positive correlations were present between FFM and brain glucose levels (r=0.80, p < 0.001,) as well as FFM and the ratio of brain glucose transport to cerebral metabolic rate (Tmax/CMRgl) (r = 0.60, p = 0.02). Conclusion: Greater FFM is associated with higher brain glucose uptake and Tmax/CMRgl. While individuals with obesity have greater fat mass and FFM, the strong positive correlation between FFM but not fat mass with brain glucose levels suggest that future studies examining the effects of obesity on brain glucose metabolism should also include measures of body composition. Future research is needed to identify which mechanisms underly the relationship between FFM and brain metabolism. Disclosure V. Burnette: None. F. Gunawan: None. B.C. Matson: None. A. Coppoli: Consultant; Ended; Merck Sharp & Dohme Corp. G.F. Mason: Consultant; Ended; Merck Sharp & Dohme Corp. Consultant; Current; Leal Therapeutics. J.J. Hwang: None. Funding National Institutes of Health (DK123227)