Abstract
BackgroundBoth hepatitis C virus (HCV) infection and adiponectin are critically involved in metabolism. The reversal and associations of altering adiponectin levels after sustained virological responses (SVRs) following direct-acting antivirals (DAA) in HCV-infected patients remained elusive.MethodsA joint study was conducted in a prospective cohort of 427 HCV-infected patients and a line of HCV core transgenic mice.ResultsOf 427, 358 had completed a course of DAA therapy and 353 had SVRs. At baseline, male sex (95% CI β: − 1.44 to − 0.417), estimated glomerular filtration rate (eGFR) (− 0.025 to − 0.008), triglycerides (− 0.015 to − 0.005), and fibrosis-4 levels (0.08–0.297) were associated with adiponectin levels; BMI (0.029–0.327) and triglycerides levels (0.01–0.03) were associated with homeostatic model assessment for insulin resistance (HOMA-IR) in HCV-infected patients. At 24-week post-therapy, in SVR patients, male sex (− 1.89 to − 0.5) and eGFR (− 0.02 to − 0.001) levels were associated with adiponectin levels, levels of BMI (0.094–0.335) and alanine transaminase (0.018–0.078) were associated with HOMA-IR; compared with baseline levels, adiponectin levels decreased (6.53 ± 2.77 vs. 5.45 ± 2.56 μg/mL, p < 0.001). In 12-month-old HCV core transgenic mice with hepatic steatosis, triglyceride levels (0.021–0.111) were associated with adiponectin levels, and hepatic adipopnectin expression was comparable with that of control mice.ConclusionsTriglycerides and hepatic fibrosis are associated with HCV-specific alteration of adiponectin levels, and adiponectin may affect insulin sensitivity through triglycerides during HCV infection. In DAA-treated patients, after SVR, adiponectin levels decreased and the linking function of triglycerides between adiponectin and insulin sensitivity vanished. Moreover, HCV core with hepatic steatosis might affect extrahepatic adiponectin expression through triglycerides.
Highlights
Both hepatitis C virus (HCV) infection and adiponectin are critically involved in metabolism
While we stratified the patients with baseline insulin resistance (IR), non-HCV G123 were positively associated with homeostatic model assessment for insulin resistance (HOMA-IR) among those with baseline IR (Additional file 1: Table S2); body mass index (BMI) levels were associated with HOMA-IR levels among those without baseline IR (Additional file 1: Table S3)
Post‐therapy associations in sustained virological responses (SVRs) patients At 24 weeks post-therapy, among 353 SVR patients (Fig. 1), male sex and estimated glomerular filtration rate (eGFR) were negatively associated with adiponectin levels (Table 4); levels of BMI and ALT were positively associated with HOMA-IR (Table 5)
Summary
Both hepatitis C virus (HCV) infection and adiponectin are critically involved in metabolism. The rever‐ sal and associations of altering adiponectin levels after sustained virological responses (SVRs) following direct-acting antivirals (DAA) in HCV-infected patients remained elusive. The reversal of HCV-associated metabolic alterations after sustained virological response (SVR) following interferon-based studies had been well demonstrated [3, 5,6,7,8,9,10]. With the advent of direct-acting antivirals (DAAs), which target specific proteins of HCV during its life cycle [14], antiHCV treatment has resulted in a high cure rate with a short treatment duration in patients with chronic HCV infection (CHC), and the reversal of HCV-associated metabolic alterations might not be biased by any interferon-related effects
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