In hepatocytes, the calcium (Ca+) concentrations play an important role in the cellular function. In this setting, studies have demonstrated that calcium plays an important role in the development of Non-alcoholic fatty liver disease (NAFLD). However, few therapies are efficient to treat the lipid accumulation in the liver. Thus, the IP3Rs are impotent intracellular regulators of calcium fluxes. Therefore, diabetic mice have increased IP3R-I activity suggesting the role IP3R-I in lipids metabolic liver. In this grant we will test the chronic excercise training will result in increases in plasma glucagon concentrations which in turn will result in increases hepatic mitochondrial oxidation rates by signaling through the InsP3R-I receptor. Next we will perform chronic exercise training in HFD IP3R-I KO mice in order to determine whether liver calcium signaling is required to mediate the effect of exercise to improve hepatic and/or whole-body insulin sensitivity with exercise training.
News published in Agência FAPESP Newsletter about the scholarship: