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. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Hepatology. 2011 Dec;54(6):1966–1974. doi: 10.1002/hep.24645

Figure 4.

Figure 4

Nuclear receptor-mediated pathways in chronic hepatitis C patients. (1) Fat influx and efflux. FATP and CD36 are involved in fatty acid uptake and MTP is important to VLDL secretion. The expression levels of FATP5, FATP2, and MTP are up-regulated in livers with chronic hepatitis C infection compared with controls. (2) Fatty acid synthesis and oxidation. SREBP-1c and PPARα are the key regulators of fatty acid synthesis and oxidation. Their expression is down-regulated in livers with chronic hepatitis C infection compared with controls. (3) Glucose uptake. GLUT2 mediates facilitated glucose uptake. Its expression was up-regulated in livers with chronic hepatitis C infection compared with controls, but de novo fatty acid synthesis was not up-regulated. (4) Bile acid synthesis and uptake. CYP7A1 catalyzes the rate-limiting step in cholesterol catabolism and bile acid biosynthesis and NTCP is involved in hepatic sodium/bile acid uptake. Expression of both genes was up-regulated in livers with chronic hepatitis C infection compared with controls. Bile acids enhance genotype 1 HCV replication in an HCV-replication cell model (38, 39). (5) SHP plays a key role in the regulation of hepatic lipid metabolism (37, 55). SHP was up-regulated in livers with chronic hepatitis C infection compared with controls, but it was accompanied by up-regulated expression of CYP7A1, NTCP, and MTP. Gene names in yellow indicate expression increase in hepatitis C patients compared with controls. Gene names in white indicate expression decrease in hepatitis C patients compared with controls. Small arrows indicate the direction of the regulatory pathways. Big arrows suggest pathways are stimulated in hepatitis C patients compared with controls. X: The inhibitory function is compromised in hepatitis C patients.