Review Article

Nutrition and Nonalcoholic Fatty Liver Disease: The Significance of Cholesterol

Figure 1

Expression profile of lipid metabolism-associated factors in nonalcoholic fatty liver disease (NAFLD). The established pathophysiological pathways in NAFLD involve increased delivery of fatty acids to the liver and increased SREBP-1c signaling because of cholesterol overload and insulin resistance. ABCG5/G8: ATP-binding cassette G5/G8; ACC: acetyl-CoA carboxylase; AdipoR: adiponectin receptor; ADRP: adipose differentiation-related protein; AMPK: AMP-activated protein kinase; ApoB: apolipoprotein B; CM: chylomicron; CPT-1: carnitine palmitoyltransferase-1; DGAT1: diacylglycerol acyltransferase 1; FAS: fatty acid synthase; HMGR: HMG-CoA reductase; HSL: hormone sensitive lipase; IR: insulin receptor; IRS2: insulin receptor substrate 2; LDLR: LDL receptor; LXRα: liver X receptor α; MTP: microsomal triglyceride transfer protein; NPC1L1: Niemann-Pick C1-like 1; PPARα: peroxisome proliferator-activated receptor α; SREBP: sterol regulatory element-binding protein; TNFα: tumor necrosis factor α; TNFR: TNF receptor.
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