title: Prevalence of abnormal glycometabolism in treatment-naive patients with hepatitis C virus infection in a Chinese Han population.
abstract: OBJECTIVE
  The hepatitis C virus (HCV) may promote pancreatic β-cell apoptosis-like cell death through a caspase 3-dependent pathway, initiating the onset of type 2 diabetes mellitus (T2DM); however, the risk factors for development of T2DM and other abnormal glycometabolic factors in HCV patients of the Chinese Han ethnicity have been poorly explored.
  
  
  METHODS
  A total of 947 patients Chinese Han patients with confirmed HCV infection were enrolled in a multicenter study in order to examine the genetic and physiological parameters associated with the onset of abnormal glycometabolic conditions, including T2DM and prediabetes.
  
  
  RESULTS
  HCV genotype 1b and host interleukin-28B CC genotype were most commonly observed. A total of 145 (15.3%) patients were diagnosed with T2DM and prediabetes. Elevated age, waist circumference, smoking duration, and systolic and diastolic blood pressure were shown to increase risks for abnormal glycometabolism. Liver dysfunction was shown to have positive correlations with abnormal glycometabolism in HCV patients. Genome-wide association studies indicated that certain genetic encoding inosine triphosphatase polymorphs (rs6051702) were associated with elevated risks for abnormal glycometabolism. Coupled with previous research data, it is likely that abnormal glycometabolism may be a useful predictor of risk for poor response to antiviral therapies and treatment-induced complications, such as anemia, in treatment naïve patients.
  
  
  CONCLUSIONS
  Abnormal glycometabolism and other such complications of HCV and HCV treatment may share critical metabolic and genetic pathways, providing potentially novel targets for future antiviral therapies for treatment resistant HCV genotypes.
authors.affiliation: Peking University People's Hospital, Beijing Key Laboratory for Hepatitis C and Immunotherapy for Liver Disease, Peking University Hepatology Institute, Beijing, China.
authors.forename: Huiying
authors.initials: H
authors.lastname: Rao
authors.forename: Lai
authors.initials: L
authors.lastname: Wei
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.forename: Ruifeng
authors.initials: R
authors.lastname: Yang
authors.forename: Haiying
authors.initials: H
authors.lastname: Zhang
authors.forename: Jia
authors.initials: J
authors.lastname: Shang
authors.forename: Hong
authors.initials: H
authors.lastname: Chen
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Qing
authors.initials: Q
authors.lastname: Xie
authors.forename: Zhiliang
authors.initials: Z
authors.lastname: Gao
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Jia
authors.initials: J
authors.lastname: Wei
authors.forename: Jianning
authors.initials: J
authors.lastname: Jiang
authors.forename: Yongtao
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000328:Adult; D044466:Asian People; D002681:China / Q000453:epidemiology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology* / Q000209:etiology* / Q000235:genetics; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000150:complications* / Q000453:epidemiology* / Q000235:genetics / Q000821:virology; D006801:Humans; D007372:Interferons; D007378:Interleukins / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011236:Prediabetic State / Q000453:epidemiology* / Q000209:etiology* / Q000235:genetics; D015995:Prevalence; D000095022:Interferon Lambda
chemical_list: D007372:Interferons; D007378:Interleukins; C000624353:interferon-lambda, human; D000095022:Interferon Lambda
keywords: glycometabolism; hepatitis C virus (HCV); inosine triphosphatase (ITPA)