BACKGROUND: Obesity is recognized as a cofactor in hepatitis C (HCV) liver injury. Adipokines may be the link between increasing body mass index (BMI) and disease progression in HCV. Adiponectin is an anti-inflammatory adipokine that is present in serum in a range of multimeric forms that appear to have different metabolic functions. METHODS: We studied 30 male patients with untreated chronic HCV (15 each with genotypes 1 and 3) and 12 controls. The three groups were matched for age and BMI. Total adiponectin and high (HMW) and low (LMW) molecular weight adiponectin multimers were measured. The relationships between adiponectin, BMI, insulin sensitivity, and liver histology were examined. RESULTS: Genotype 3 was associated with greater hepatic steatosis and inflammation than genotype 1. Patients with genotype 1 were less insulin sensitive than genotype 3, who had similar insulin sensitivity to controls. Insulin resistance was associated with a decrease in total and HMW adiponectin in both HCV and controls, while LMW adiponectin was unchanged. When the effect of genotype was examined, this association was present with genotype 3 but not genotype 1 infection. CONCLUSIONS: These data demonstrate that the relationship between insulin resistance and adiponectin is similar in controls and patients with genotype 3 but not genotype 1 infection. The greater degree of insulin resistance in genotype 1 appears to be a genotype-specific effect.
BACKGROUND: Obesity is recognized as a cofactor in hepatitis C (HCV) liver injury. Adipokines may be the link between increasing body mass index (BMI) and disease progression in HCV. Adiponectin is an anti-inflammatory adipokine that is present in serum in a range of multimeric forms that appear to have different metabolic functions. METHODS: We studied 30 male patients with untreated chronic HCV (15 each with genotypes 1 and 3) and 12 controls. The three groups were matched for age and BMI. Total adiponectin and high (HMW) and low (LMW) molecular weight adiponectin multimers were measured. The relationships between adiponectin, BMI, insulin sensitivity, and liver histology were examined. RESULTS: Genotype 3 was associated with greater hepatic steatosis and inflammation than genotype 1. Patients with genotype 1 were less insulin sensitive than genotype 3, who had similar insulin sensitivity to controls. Insulin resistance was associated with a decrease in total and HMWadiponectin in both HCV and controls, while LMW adiponectin was unchanged. When the effect of genotype was examined, this association was present with genotype 3 but not genotype 1 infection. CONCLUSIONS: These data demonstrate that the relationship between insulin resistance and adiponectin is similar in controls and patients with genotype 3 but not genotype 1 infection. The greater degree of insulin resistance in genotype 1 appears to be a genotype-specific effect.
Authors: S Mazaki-Tovi; R Romero; J P Kusanovic; O Erez; E Vaisbuch; F Gotsch; P Mittal; G N Than; C Nhan-Chang; T Chaiworapongsa; S Edwin; N Camacho; J K Nien; S S Hassan Journal: J Matern Fetal Neonatal Med Date: 2008-11