Genetic polymorphisms of adiponectin and tumor necrosis factor-alpha and nonalcoholic fatty liver disease in Chinese people

Authors: Wong, Vincent Wai-Sun; Wong, Grace Lai-Hung; Tsang, Steven Woon-Choi1; Hui, Alex Yui; Chan, Anthony Wing-Hong2; Choi, Paul Cheung-Lung2; So, Wing-Yee3; Tse, Ada Mei-Ling; Chan, Francis Ka-Leung; Sung, Joseph Jao-Yiu; Chan, Henry Lik-Yuen

Source: Journal of Gastroenterology and Hepatology, Volume 23, Number 6, June 2008 , pp. 914-921(8)

Publisher: Blackwell Publishing

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Abstract:

Background and Aim: 

Hypoadiponectinemia and high tumor necrosis factor-alpha (TNF-α) levels are associated with the development of nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate the genetic polymorphisms of adiponectin and TNF-α in Chinese NAFLD patients and their association with disease severity. Methods: 

Seventy-nine patients with histology-proven NAFLD (61 with simple steatosis and 18 with stage 2-4 fibrosis) and 40 controls were tested for the nucleotide polymorphisms at adiponectin −11 391, −11 377, +45, and +276 and TNF-α promoters −863, −308, and −238. Results: 

There was no significant deviation in the adiponectin and TNF-α gene polymorphisms between NAFLD patients and controls, or between patients with simple steatosis and those with stage 2-4 fibrosis. NAFLD patients with −11377G and +45G at the adiponectin gene were more likely to have hypertriglyceridemia. On multivariate analysis, older age, higher body mass index, and higher fasting glucose were independent factors associated with stage 2-4 fibrosis in NAFLD patients. Conclusions: 

Adiponectin and TNF-α gene polymorphisms were not shown to be associated with NAFLD or significant fibrosis in Chinese people. The adiponectin −11377G and +45G alleles were associated with hypertriglyceridemia in NAFLD patients. Since the current study is not adequately powered to detect smaller differences in allele frequencies, larger-sized studies in different ethnic groups are required.

Keywords: adiponectin; diabetes mellitus; fatty liver; metabolic syndrome X; tumor necrosis factor-alpha

Document Type: Research article

DOI: 10.1111/j.1440-1746.2008.05344.x

Affiliations: 1: Department of Medicine, Tseung Kwan O Hospital, Hong Kong 2: Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, and 3: Department of Medicine and Therapeutics,

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