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Acta Biochimica et Biophysica Sinica Advance Access published online on November 9, 2009
Acta Biochimica et Biophysica Sinica, doi:10.1093/abbs/gmp097
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Hyperhomocysteinemia stimulates hepatic glucose output and PEPCK expression

Xue Yu1, Youguang Huang2, Qiang Hu3 and Lanqing Ma4,*

1 Department of Cardiology, Beijing Hospital, Beijing 100730, China
2 Department of Biochemistry, Kunming Medical College, Kunming 650031, China
3 Department of Emergency Medicine, The Second Affiliated Hospital, Kunming Medical College, Kunming 650101, China
4 Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical College, Kunming 650032, China

* Correspondence address. Tel: +86-871-5324888; Fax: +86-871-5322480; E-mail: lanqingma75{at}yahoo.cn


  Abstract

Homocysteine is an intermediate in the sulfur amino acid metabolism. Recent studies suggested that there might be links between hyperhomocysteinemia and insulin resistance. In the present study, we investigated the effect of homocysteine on glucose metabolism. We demonstrated that the levels of insulin were significantly higher in mice with hyperhomocysteinemia than those in the normal mice after administration of glucose. The effect of insulin on glucose output was significantly blocked in the homocysteine-treated hepatocytes. In addition, the expression of phosphoenolpyruvate carboxykinase (PEPCK) gene was elevated in the liver of mice with hyperhomocysteinemia and primary mouse hepatocytes treated with homocysteine. The action of homocysteine was suppressed by H89, a protein kinase A (PKA) inhibitor. Thus, hyperhomocysteinemia may be considered as a risk factor that contributes to the development of insulin resistance with respect to elevated glucose output and upregulation of PEPCK, probably via the PKA pathway. Our study provides a novel mechanistic explanation for the development of insulin resistance in hyperhomocysteinemia.

Keywords    homocysteine; insulin resistance; phosphoenolpyruvate carboxykinase (PEPCK); protein kinase A

Received: July 21, 2009; Accepted: September 15, 2009
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