Klf16, a member of the Kruppel-like factor (KLF) family, is involved in multiple biological processes. It is related to adipose tissue development and/or glucose metabolism, and also plays roles in various diseases [2]. In the liver, it targets peroxisome proliferator-activated receptor α (PPARα), closely linking hepatic lipid homeostasis and redox balance [1].

In liver-specific Klf16-deficient mice fed a high-fat diet, fatty acid oxidation was impaired, mitochondrial stress and ROS burden were aggravated, leading to advanced hepatic steatosis and insulin resistance [1]. In contrast, Klf16 overexpression reduced lipid deposition and improved insulin resistance in db/db and HFD mice by directly binding to the PPARα promoter [1].

In conclusion, Klf16 plays a crucial role in regulating hepatic lipid catabolism, which is significant for maintaining normal liver function and preventing insulin resistance and hepatic steatosis. The study of Klf16-deficient mouse models has provided valuable insights into the molecular mechanisms underlying these disease-related processes in the liver.