Fig. 4

Proposed mechanism for α-MG action against fat infiltration of the liver. High fat diet in an obesity setting, leads to overload of FFAs in hepatocytes. Consequently, there occurs increased ROS production and lipid peroxidation in the liver, which further damage the antioxidant enzymes and mitochondria. Mitochondrial damage leads to cyt c and Ca²⁺ release from mitochondria, thereafter cyt c binds to Apaf-1 and activates apoptosis via caspases 9 and 3 factors. Apoptosis implies rapid death of hepatocytes hence reduced clearance of fat deposits. On the other hand, mitochondrial damage in turn leads to a decreased mitochondrial oxidative capacity, including β-oxidation and ATP production, resulting in TG accumulation in the liver. α-MG limits hepatic TG accumulation through enhanced anti-oxidative capacity and hepatic mitochondrial oxidative metabolic capacity and inhibition of mitochondrial pathway of apoptosis, which may confer decreased hepatic steatosis risk. ROS: reactive oxygen species; Ca²⁺ : calcium ; cyt c : cytochrome c ; TG: triglyceride