BACKGROUND: Several clinical studies have suggested a possible link between chronic hepatitis caused by hepatitis C virus (HCV) and the development of diabetes mellitus. We investigated the association between liver fibrosis and glucose intolerance in HCV-infected patients by measuring insulin sensitivity and beta-cell function. METHOD: A total of 83 chronic HCV-infected patients were recruited into this study. We evaluated insulin sensitivity and beta-cell function of all patients in a fasting state (homeostasis model assessment of insulin resistance [HOMA-R] and homeostasis model assessment of beta-cell function [HOMA-beta]) and after an oral load of 75 g glucose (whole-body insulin sensitivity index [WBISI] and Delta-insulin/Delta-glucose 30). RESULTS: In a multivariate analysis, severe fibrosis was the only independent factor associated with insulin resistance. There were significant differences in both HOMA-R (P= 0.0063) and WBISI (P= 0.0159) between patients with mild fibrosis (N = 34) and those with severe fibrosis (N = 49). Although HOMA-beta was increased significantly in the subjects with severe fibrosis compared with those with mild fibrosis (P= 0.0169), Delta-insulin/Delta-glucose 30 showed no significant difference in stage of liver fibrosis, suggesting an uncertain association between liver fibrosis and beta-cell function. CONCLUSION: Our findings suggest that the development of liver fibrosis is associated with insulin resistance in HCV-infected patients.
BACKGROUND: Several clinical studies have suggested a possible link between chronic hepatitis caused by hepatitis C virus (HCV) and the development of diabetes mellitus. We investigated the association between liver fibrosis and glucose intolerance in HCV-infectedpatients by measuring insulin sensitivity and beta-cell function. METHOD: A total of 83 chronic HCV-infectedpatients were recruited into this study. We evaluated insulin sensitivity and beta-cell function of all patients in a fasting state (homeostasis model assessment of insulin resistance [HOMA-R] and homeostasis model assessment of beta-cell function [HOMA-beta]) and after an oral load of 75 g glucose (whole-body insulin sensitivity index [WBISI] and Delta-insulin/Delta-glucose 30). RESULTS: In a multivariate analysis, severe fibrosis was the only independent factor associated with insulin resistance. There were significant differences in both HOMA-R (P= 0.0063) and WBISI (P= 0.0159) between patients with mild fibrosis (N = 34) and those with severe fibrosis (N = 49). Although HOMA-beta was increased significantly in the subjects with severe fibrosis compared with those with mild fibrosis (P= 0.0169), Delta-insulin/Delta-glucose 30 showed no significant difference in stage of liver fibrosis, suggesting an uncertain association between liver fibrosis and beta-cell function. CONCLUSION: Our findings suggest that the development of liver fibrosis is associated with insulin resistance in HCV-infectedpatients.
Authors: Alexander J Thompson; Keyur Patel; Wan-Long Chuang; Eric J Lawitz; Maribel Rodriguez-Torres; Vinod K Rustgi; Robert Flisiak; Stephen Pianko; Moises Diago; Sanjeev Arora; Graham R Foster; Michael Torbenson; Yves Benhamou; David R Nelson; Mark S Sulkowski; Stefan Zeuzem; Erik Pulkstenis; G Mani Subramanian; John G McHutchison Journal: Gut Date: 2011-08-26 Impact factor: 23.059
Authors: Diego Garcia-Compean; Joel Omar Jaquez-Quintana; Jose Alberto Gonzalez-Gonzalez; Hector Maldonado-Garza Journal: World J Gastroenterol Date: 2009-01-21 Impact factor: 5.742
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Authors: Diego García-Compeán; Joel Omar Jáquez-Quintana; Fernando Javier Lavalle-González; José Alberto González-González; Linda Elsa Muñoz-Espinosa; Jesús Zacarías Villarreal-Pérez; Héctor J Maldonado-Garza Journal: World J Gastroenterol Date: 2014-06-14 Impact factor: 5.742