The relationship between insulin resistance and adiponectin gene expression in nonalcoholic fatty liver disease.
- Author:
Hui YANG
1
;
Yu-yuan LI
;
Yu-qiang NIE
;
Yong-jian ZHOU
;
Yan-lei DU
;
Wei-hong SHA
;
Yong HONG
Author Information
- Publication Type:Journal Article
- MeSH: Adiponectin; genetics; metabolism; Adipose Tissue; metabolism; Body Mass Index; Case-Control Studies; Fatty Liver; genetics; metabolism; Female; Gene Expression; Humans; Insulin; metabolism; Insulin Resistance; Lipid Metabolism; Male; Obesity; genetics; metabolism
- From: Chinese Journal of Hepatology 2007;15(7):525-528
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the relationship between insulin resistance (IR) and adiponectin gene expression in patients with nonalcoholic fatty liver disease (NAFLD).
METHODSSubcutaneous (SC) and omental (OM) adipose tissues were obtained from 21 NAFLD patients with obesity (n=10) and nonobesity (n=11) and also from 24 subjects (without NAFLD) with obesity (n=11) and nonobesity (n=13) who served as controls. Adiponectin mRNA expression levels in subcutaneous and omental adipose tissues were measured using SYBR Green I quantitative real-time PCR. The levels of plasma adiponectin and insulin were measured with ELISA. IR was estimated using the homeostasis assessment (HOMA).
RESULTSThe scores of HOMA-IR levels of the NAFLD patients and the controls with obesity and nonobesity were: 3.0+/-0.8, 2.8+/-0.9, 2.0+/-0.6, 1.2+/-0.5 respectively. The relative mRNA expression of adiponectin and blood adiponectin levels in NAFLD patients differed significantly from those of the controls. The HOMA-IR negatively correlated with the adiponectin mRNA expression levels of adipose tissues (r = -0.5) and blood adiponectin; it positively correlated with body mass index (r = 0.4), waist-hip-ratio (r = 0.4) and serum triglyceride (r = 0.3), but did not correlate with serum total cholesterol (r = 0.2).
CONCLUSIONIR of NAFLD patients was linked to low adiponectin gene expression in their adipose tissues. This finding suggests that low adiponectin gene expression may play a role in the pathogenesis of insulin resistance and NAFLD.