*Therapeutic Approach to NAFLD-NASH DOI: http://dx.doi.org/10.5772/intechopen.107487*

lobular inflammation, and steatosis in a meta-analysis that compared the use of Thiazolidinediones to placebo in 334 individuals, but no significant improvement of fibrosis was detected. The favorable benefits were reversed following drug termination, which is proof that a prolonged course of treatment is necessary to provide a substantial benefit [26, 27].

Apart from PPARγ agonists, there also are other members of the drug family (PPARα and PPARδ) agonists which are expressed mostly in oxidative tissues and are deeply involved in mitochondrial biogenesis and metabolism, fatty acid oxidation, ketogenesis, and fatty acid uptake-triglyceride metabolism. Elafribranor, a dual PPARα—PPARδ agonist, has been proven in animal models to enhance lipid and insulin metabolism and lessen hepatic inflammation and fibrosis. In animal models, the drug Lanifribranor has demonstrated improved glucose metabolism and decreased steatosis. Saroglitazar, a dual PPARα/γ agonist, also increased insulin sensitivity in people with type 2 diabetes. It also decreased hepatic steatosis and inflammation while preventing fibrosis in animal models. All of these agents are tested in ongoing trials [28–30].
