Journal of Glycomics & Lipidomics
Open Access
ISSN: 2153-0637
+44 1223 790975
ISSN: 2153-0637
+44 1223 790975
Chao Zhou1, Hongmei Jia1, Huikun Wu2, Yuanming Ba2 and Zhongmei Zou1
1Chinese Academy of Medical Sciences & Peking Union Medical College, China 2Hubei Provincial Hospital of TCM, China
Posters-Accepted Abstracts: J Glycomics Lipidomics
Chronic hepatitis B virus (HBV) infection is a huge burden to public health. An estimate 375 million people are chronically HBV infected worldwide. And the number of HBV infected people continues to increase with 4.5 million every year. Patients with HBV infection are apt to develop advanced liver disease such as cirrhosis and hepatocellular carcinoma. But there is a noteworthy disparity of HBV treatment in current clinical practice which is largely attributed to the poor understanding on the pathogenesis of HBV-mediated liver injury. Serum contains a large variety of small-molecular metabolites which are closely related to physiological states. Comprehensive analysis of these metabolites can hence facilitate the understanding of mechanism underlying the disease. Therefore, to decipher the mechanism underlying HBV-mediated liver injury, mass spectrometry-based metabolomic analysis was carried out in patients with chronic hepatitis B (CHB), liver failure (LF) and healthy controls. As a result, significantly decreasing of lysophosphatidylcholines accompanied with increasing of bile acids were found in patients with CHB and LF. In addition, to mimic the clinical symptoms of the injury, two animal models were replicated, including mice model with immune-mediated liver injury induced by concanavalin A and rats model with chemical liver injury induced by CCl4. Metabolic profiling analysis of animal models also showed a similar alteration in lysophosphatidylcholines and bile acids. Therefore, our cross-species analysis of serum provides evidence for a common architecture in liver injury and present disorders of glycerophospholipid and bile acid metabolism are the key players in pathogenesis of the liver injury.
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