PPAR Research / 2009 / Article / Fig 3

Review Article

Regulation of Bile Acid and Cholesterol Metabolism by PPARs

Figure 3

Reverse cholesterol transport. In the intestine, dietary uptake of cholesterol is mediated by NPC1L1. ABCG5/G8 effluxes sitosterols and cholesterol back to the intestine lumen and limits intestinal sterol absorption. Oxysterols activate LXR, which induces ABCA1 and ABCG1 to transport cholesterol to ApoA1 and HDL, respectively. PPAR activation reduces NPC1L1 and fractional cholesterol absorption, and may promote cholesterol secretion by stimulating CYP27A1 and LXR activation of ABCA1 and ABCG1. In macrophages, LDLR and CD36 mediate LDL and oxidized-LDL uptake, respectively. CYP27A1 converts cholesterol into 27-hydroxycholesterol, which may activate LXR and cholesterol efflux via ABCA1 and ABCG1. Cholesterol can also be secreted in the form of 27-hydroxycholesterol. PPAR induces CYP27A1 and LXR, and positively regulates the cholesterol efflux from macrophages. PPAR induces ApoA1 and inhibits CETP, and thus increases circulating HDL-C levels.

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