Research Assistant professor Texas Tech University Lubbock, Texas, United States
Objectives: Overconsumption of palatable food is a major contributor to the recent spike in obesity prevalence. Circulating levels of branched-chain amino acids (BCAAs) are observed in both human and animal models of obesity and type 2 diabetes. Low protein and/or BCAA-restricted diets have shown to induce the expression of a hepatokine called fibroblast growth factor (FGF21), which negatively regulates simple sugar intake and sweet preference in mice. Whether or not BCAAs can alter reward functions to increase preference for palatable foods and the role of FGF21 in this process have not been explored. Therefore, we tested the effects of a short-term BCAA exposure on the consumption of palatable sucrose solution and plasma FGF21 levels.
Methods: 8-week-old male C57Bl/6 mice were assigned to two weight-matched groups to receive intraperitoneal injections of either saline or BCAAs (225 nM; N=5/group) twice a day for 7 consecutive days. Before and after intervention, their 10% sucrose intake was measured for two days. Following the completion of the study, mice were sacrificed for plasma and tissue collection. Daily body weight and food intake were measured throughout the study. Blood glucose was checked by a hand-held glucometer, and plasma BCAAs and FGF21 were measured by enzymatic and ELISA assays, respectively.
Results: Plasma BCAA levels tended to be higher in the BCAA group compared to saline group as expected. While sucrose intake was identical between groups at baseline, BCAA treatment increased sucrose intake that was independent of body weight, food intake, or blood glucose. This was associated with lower plasma FGF21 in BCAA group compared to saline group.
Conclusions: Our findings suggest that a short-term supplementation of BCAAs may promote indulgence in palatable sucrose solution, and this may be potentially related to the reduction in plasma FGF21 levels. Determining the long-term effects of BCAAs on sucrose preference and FGF21 as a possible mediator is warranted. Our study sheds light on the novel role of BCAAs in food reward.
Funding Sources: Diabetes Action Foundation, Alzheimer’s Association
