Association Between Liver Fibrosis and Insulin Sensitivity in Chronic HCV
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 β-cell function.
Method: A total of 83 chronic HCV-infected patients were recruited into this study. We evaluated insulin sensitivity and β-cell function of all patients in a fasting state (homeostasis model assessment of insulin resistance [HOMA-R] and homeostasis model assessment of β-cell function [HOMA-β]) and after an oral load of 75 g glucose (whole-body insulin sensitivity index [WBISI] and Δ-insulin/Δ-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-β was increased significantly in the subjects with severe fibrosis compared with those with mild fibrosis (P = 0.0169), Δ-insulin/Δ-glucose 30 showed no significant difference in stage of liver fibrosis, suggesting an uncertain association between liver fibrosis and β-cell function.
Conclusion: Our findings suggest that the development of liver fibrosis is associated with insulin resistance in HCV-infected patients.
It has been reported that up to one-third of patients with chronic liver disease caused by hepatitis C virus (HCV) infection develop type 2 diabetes mellitus (DM). This incidence is much higher than that observed in the general population and in patients with other chronic liver diseases, such as hepatitis B virus (HBV), alcoholic liver disease, and autoimmune liver disease. Moreover, HCV seropositivity in patients with DM appears to be higher than in the general population. Post-liver-transplantation DM also appears to be high among patients with HCV. Because insulin resistance plays a key role in the development of type 2 DM, several clinical studies have investigated insulin resistance in HCV-infected patients, where insulin resistance is associated with progression of liver fibrosis, although the mechanism is still not fully understood.
In the present study, to identify the independent factor(s) relevant to insulin resistance in HCV-infected patients, we conducted a detailed comparison of various physical and biochemical parameters between patients with and without insulin resistance, and performed univariate and multivariate analyses. In addition, we also clarified the differences of four indices concerning insulin sensitivity and β-cell function, homeostasis model assessment of insulin resistance (HOMA-R), whole-body insulin sensitivity index (WBISI), homeostasis model assessment of β-cell function (HOMA-β), and Δ-insulin/Δ-glucose 30, between patients with mild fibrosis and those with severe fibrosis.
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 β-cell function.
Method: A total of 83 chronic HCV-infected patients were recruited into this study. We evaluated insulin sensitivity and β-cell function of all patients in a fasting state (homeostasis model assessment of insulin resistance [HOMA-R] and homeostasis model assessment of β-cell function [HOMA-β]) and after an oral load of 75 g glucose (whole-body insulin sensitivity index [WBISI] and Δ-insulin/Δ-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-β was increased significantly in the subjects with severe fibrosis compared with those with mild fibrosis (P = 0.0169), Δ-insulin/Δ-glucose 30 showed no significant difference in stage of liver fibrosis, suggesting an uncertain association between liver fibrosis and β-cell function.
Conclusion: Our findings suggest that the development of liver fibrosis is associated with insulin resistance in HCV-infected patients.
It has been reported that up to one-third of patients with chronic liver disease caused by hepatitis C virus (HCV) infection develop type 2 diabetes mellitus (DM). This incidence is much higher than that observed in the general population and in patients with other chronic liver diseases, such as hepatitis B virus (HBV), alcoholic liver disease, and autoimmune liver disease. Moreover, HCV seropositivity in patients with DM appears to be higher than in the general population. Post-liver-transplantation DM also appears to be high among patients with HCV. Because insulin resistance plays a key role in the development of type 2 DM, several clinical studies have investigated insulin resistance in HCV-infected patients, where insulin resistance is associated with progression of liver fibrosis, although the mechanism is still not fully understood.
In the present study, to identify the independent factor(s) relevant to insulin resistance in HCV-infected patients, we conducted a detailed comparison of various physical and biochemical parameters between patients with and without insulin resistance, and performed univariate and multivariate analyses. In addition, we also clarified the differences of four indices concerning insulin sensitivity and β-cell function, homeostasis model assessment of insulin resistance (HOMA-R), whole-body insulin sensitivity index (WBISI), homeostasis model assessment of β-cell function (HOMA-β), and Δ-insulin/Δ-glucose 30, between patients with mild fibrosis and those with severe fibrosis.
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