Skip to main content
. Author manuscript; available in PMC: 2019 Jun 26.
Published in final edited form as: Liver Res. 2018 Dec 20;2(4):209–215. doi: 10.1016/j.livres.2018.12.001

Fig. 2. Upstream regulators and downstream targets of PPARγ2-mediated hepatic lipid homeostasis.

Fig. 2

Increased ghrelin by chronic HFD consumption induces Pparg2 gene expression through mTOR signaling. Similarly, external stresses (i.e., nutritional stress) induce or inhibit Pparg2 transcription via AP1 depending on the specific heterodimer formation. Increased PPARγ2 activates downstream target genes such as LPL and CD36 for FA uptake, aP2 for intracellular FA trafficking, MOGAT1 for synthesis of diacylglycerol, and ADRP and FSP27 for lipid droplet accumulation. These targets are not major genes in hepatic TG synthesis during normal conditions. However, when PPARγ2 expression is increased by HFD feeding, these target genes contribute to lipid accumulation in the liver. Abbreviations: PPARγ2, peroxisome proliferator-activated receptor gamma 2; Chylm, chylomicron remnants; FFA, free fatty acids; FA-CoA, fatty acyl-Coenzyme A; MG, monoacylglycerol; DG, diacylglycerol; TG, triacylglycerol; GHRL, ghrelin; GHSR1, ghrelin receptor; LPL, lipoprotein lipase; CD36, cluster of differentiation 36; aP2, adipocyte protein 2; AP1, activator protein 1; mTOR, mammalian target of rapamycin; ADRP, adipose differentiation-related protein; FSP27, fat specific protein 27; MOGAT1, monoacylglycerol O-acyltransferase 1.