They concluded that SIRT5 regulates both cytosolic and mitochondrial protein malonylation with glycolysis as a major target, linking Kmal with glucose metabolism.58 Based on their research, another group constructed the hepatic Sirt5-overexpressing ob/ob mouse model to study the biological role of SIRT5 and malonylation in pathological state of obesity.196 They demonstrated that overexpression of Sirt5 results in decreased malonylation and succinylation in hepatic cells, improved cellular glycolysis, suppressed gluconeogenesis, enhanced fatty acid oxidation, and attenuated hepatic steatosis. This evidence concerns the gene SIRT5 and Obesity.