Skip to main content
. Author manuscript; available in PMC: 2022 Sep 1.
Published in final edited form as: Adv Drug Deliv Rev. 2021 Jul 24;176:113888. doi: 10.1016/j.addr.2021.113888

Figure 1. Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease (NAFLD).

Figure 1.

Various synthetic PPAR agonists are being evaluated for the treatment of NAFLD. PPAR-α activation leads to fatty acid β-oxidation in the mitochondria. The products can be later converted into ketone bodies (β-hydroxybutyrate or acetoacetate) or can be incorporated into TCA cycle as Acetyl CoA for further oxidation. PPAR- β/δ activation induces FOXO-1 transcription, which reduces hepatic gluconeogenesis and glucose uptake processes. Further, PPAR-β/δ activation suppresses inflammation by reducing IL-1β, IL-6, and NF-κB . Activation of PPAR-γ is linked to decreased hepatocyte lipogenesis and keeps HSCs in quiescent state. Dual or pan agonists targeting two or more of PPARs such as Lanifibranor has shown promising results in pre-clinical and clinical studies.