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Publication Information
Affiliation
Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pa., USA.
Authors
Afdhal N, Agudelo E, Belle SH, Bilonick RA, Block G, Brown RS Jr, Brown S, Burton JR, Callison K, Cannon N, Cline J, Conjeevaram HS, Davis P, DeMedina M, Di Bisceglie A, Donlin M, Doo E, Dougherty K, Dove L, Everhart J, Feingold E, Ferris M, Fontana RJ, Fried MW, Geahigan T, Haritos M, Harsh D, Hermitt C, Hinds M, Hoofnagle JH, Howell CD, Im K, Iuliano AD, Jeffers LJ, Kelley S, Kelsey S, Klarquist J, Kleiner DE, Koozer L, Lawlor S, Liang TJ, McPherson Baker S, Robuck P, Rosen HR, Sanda C, Schaley J, Seeff LB, Shrestha R, Smith SR, Stovel S, Straley S, Tang G, Tavis JE, Taylor MW, Terrault N, Theodore D, Thomas SB, Virahep-C Study, Wahed A, Wahed AS, Wang D, Wang P, Wei Y, Weston S, Wiley TE, Williams M, Yang H, Yao E, Yee LJ, Zacks S, Zmuda J
Studies
Citation
Iuliano AD, Feingold E, Wahed AS, Kleiner DE, Belle SH, Conjeevaram HS, Zmuda J, Liang TJ, Yee LJ, Virahep-C Study. Host genetics, steatosis and insulin resistance among African Americans and Caucasian Americans with hepatitis C virus genotype-1 infection. Intervirology 2009;52(1):49-56. Epub 2009 Apr 25.Abstract
Hepatic steatosis is the accumulation of fat in liver cells. Insulin resistance (IR) occurs when normal amounts of insulin do not stimulate insulin activity in cells. Both conditions have been described in hepatitis C virus (HCV) infection and are thought to be biologically related. This study examined the association of genetic variants with steatosis and IR among 167 African Americans and 184 Caucasian Americans with HCV genotype-1. Steatosis was defined as at least 5% of fat in cells on liver biopsy. IR was quantified as a score greater than 2 from the Homeostasis Model Assessment, version 2.2 (HOMA2-IR). Associations were investigated by estimating odds ratios separately by race. Statistically significant associations (p < 0.05) were observed for variants in interleukin-10 (IL10), leptin receptor (LEPR), interleukin-6 (IL6) and transforming growth factor beta-1 (TGF-beta1) for both outcomes. Some significant interactions were observed between IL10,LEPR and TGF-beta1 polymorphisms and HOMA2-IR scores when examining steatosis. The interaction of HOMA2-IR and IL10 was consistent in both races whereas for LEPR and TGF-beta1 the interactions were statistically significant in only one of the racial groups.These results could imply that some IL10,LEPR and TGF-beta1 polymorphisms may modify an association between steatosis and IR.