Adiponectin levels among patients with chronic hepatitis B and C infections and in response to IFN-alpha therapy.
OBJECTIVE
The study was designed to survey the change of adiponectin levels before and after interferon-alpha (IFN-alpha) therapy in patients with chronic hepatitis B and C infections.


METHODS
Twenty-one biopsy-proved patients with chronic hepatitis B (10 cases) and hepatitis C (11 cases) were given IFN-alpha for a total of 24 weeks. Fasting plasma glucose, insulin and adiponectin levels were obtained before and 12 weeks after completion of IFN-alpha therapy. Insulin suppression test was conducted before and within 1 week after IFN-alpha therapy.


RESULTS
The change of adiponectin levels differed significantly between responders (eight cases) and non-responders (13 cases) to IFN-alpha treatment (-4.8+/-2.2 vs. 0.5+/-1.0 microg/ml, P=0.03). After adjusting for age, gender and change in body mass index, the study found the change of adiponectin levels still significantly related to the response to IFN-alpha (P=0.04). When hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected patients were separately analyzed, the adiponectin levels reported a trend to decrease in HCV responders (11.9+/-3.2 vs. 10.8+/-3.0 microg/ml, P=0.02, n=4) and HBV responders (17.7+/-4.1 vs. 9.2+/-1.0 microg/ml, P=0.10, n=4). In addition, a significant decrease of steady-state plasma glucose in insulin suppression test was noted in responders (13.6+/-1.8-11.7+/-1.2 mmol/l, P=0.03), but not in non-responders (12.3+/-1.1-11.0+/-1.0 mmol/l, P=0.20), after IFN-alpha therapy.


CONCLUSIONS
IFN-alpha resulted in a decrease of serum adiponectin levels but an improvement of insulin resistance in responders to the treatment. The result contradicts previous concept of the relationship between insulin resistance and adiponectin levels. Whether and how the augmented immune response, which was supposed to result from the disappearance or the profound down-regulation of the virus or viral antigens in responders to IFN-alpha treatment, contributes to the lowering of adiponectin levels needs to be further investigated.
Lu
Jin-Ying
JY
Department of Laboratory Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Chuang
Lee-Ming
LM
Yang
Wei-Shiung
WS
Tai
Tong-Yuan
TY
Lai
Ming-Yang
MY
Chen
Pei-Jer
PJ
Kao
Jia-Horng
JH
Lee
Cha-Ze
CZ
Lee
Hsuan-Shu
HS
D052242:Adiponectin; D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D005260:Female; D019694:Hepatitis B, Chronic / Q000097:blood* / Q000188:drug therapy*; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000188:drug therapy*; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000276:immunology; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008111:Liver Function Tests; D008297:Male; D011994:Recombinant Proteins; D016896:Treatment Outcome
D052242:Adiponectin; D000998:Antiviral Agents; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins