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PubMed ID:
19401628
Public Release Type:
Journal
Publication Year: 2009
Affiliation: Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pa., USA.
DOI:
https://doi.org/10.1159/000214380
Authors:
Dove L,
Jeffers LJ,
Callison K,
Howell CD,
Williams M,
Wiley TE,
Hinds M,
Agudelo E,
Straley S,
Terrault N,
Stovel S,
Brown RS Jr,
Geahigan T,
Afdhal N,
Virahep-C Study,
Yee LJ,
Liang TJ,
Zmuda J,
Conjeevaram HS,
Belle SH,
Kleiner DE,
Wahed AS,
Feingold E,
Iuliano AD,
Kleiner DE,
Seeff LB,
Liang TJ,
Doo E,
Hoofnagle JH,
Everhart J,
Robuck P,
Yee LJ,
Wei Y,
Wahed A,
Thomas SB,
Lawlor S,
Koozer L,
Kelsey S,
Kelley S,
Im K,
Haritos M,
Cline J,
Block G,
Bilonick RA,
Belle SH,
Ferris M,
Schaley J,
Sanda C,
Taylor MW,
Weston S,
Klarquist J,
Burton JR,
Rosen HR,
Wang D,
Tang G,
Yang H,
Wang P,
Cannon N,
Donlin M,
Yao E,
Di Bisceglie A,
Tavis JE,
Brown S,
Davis P,
Dougherty K,
Shrestha R,
Zacks S,
Theodore D,
Smith SR,
Fried MW,
Harsh D,
Fontana RJ,
Conjeevaram HS,
Hermitt C,
DeMedina M,
McPherson Baker S
Studies:
Viral Resistance to Antiviral Therapy of Chronic Hepatitis C
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.
