Adiponectin and Its Receptors in Chronic Hepatitis B Patients With Steatosis in China


Di Wu 1 , Hongqi Li 8 , Guoan Xiang 3 , Liwei Zhang 4 , Lihong Li 5 , Yongmei Cao 6 , * , Jinqian Zhang 7 , *

1 Department of Ultrasound, Air Force General Hospital of PLA, Beijing, China

8 Daping Hospital,Third Military Medical University, Chongqing, China

3 Department of General Surgery, the Second People's Hospital of Guangdong Province, Guangzhou, China

4 Department of Cardiology, the First Affiliated Hospital of Chinese PLA General Hospital, Beijing, China

5 Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xian, China

6 International Mongolian Hospital, Hohhot of Inner Mongolia, Hohhot, China

7 Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, China

Corresponding Authors:

How to Cite: Wu D, Li H, Xiang G, Zhang L, Li L, et al. Adiponectin and Its Receptors in Chronic Hepatitis B Patients With Steatosis in China, Hepat Mon. 2013 ; 13(4):6065. doi: 10.5812/hepatmon.6065.


Hepatitis Monthly: 13 (4); 6065
Published Online: April 18, 2013
Article Type: Research Article
Received: May 22, 2012
Accepted: January 30, 2013


Background: HBV infection is a serious public health problem worldwide, which can contribute to the incidence of chronic hepatitis B (CHB), cirrhosis, and hepatocellular carcinoma (HCC).

Objectives: In the present report, we assessed the association between adiponectin, its receptors and hepatic steatosis, fibrosis, and inflammation with hepatitis B virus.

Patients and Methods: Liver biopsies from 89 patients with untreated chronic hepatitis B (34 steatosis vs. 55 without steatosis) were analyzed; liver biopsies from 50 healthy adults were used as control. The liver biopsies were subjected to routine histological examination, and stained immunohistochemically for adiponectin and adiponectin receptor2 (adipoR2).

Results: The two groups were found to be comparable with respect to demographic, biochemical, metabolic, histological, and viral characteristics. BMI, ?-GT, FPG, insulin, and insulin sensitivity estimated by the HOMA index were significantly higher in patients with steatosis. The viral load of HBV and HBeAg positivity was higher in patients with steatosis than those without steatosis. High serum adiponectin levels were significantly correlated with abnormal serum ALT level (vs. normal ALT, P = 0.000), and HBV genotype C (vs. genotype B, P = 0.018). In patients with chronic HBV, the insulin sensitizing adipokine adiponectin, and its receptor AdipoR2were associated with steatosis. While adiponectin may becorrelated with inflammation, adiponectin, and its receptors were not associated with viral factors.

Conclusions: Our results suggest that the role of adiponectin might be impaired in chronic hepatitis B with steatosis. Reduced hepatic expression of adiponectin and adipoR2 might be of pathophysiological relevance in CHB patients with steatosis. These findings indicated that reduced liver adiponectin expression may play an important role in the pathogenesis, and progression of CHB patients with steatosis. However, hepatic expression of adiponectin, and adipoR2 was not associated with various measures of HBV infection.

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