Apolipoprotein M

Lipids in Health and Disease

Ning Xu²  Peter Nilsson-Ehle²  Xiaoying Zhang¹  Guanghua Luo¹ 

[1] Laboratory of Molecular Medicine, The Third Affiliated Hospital, Su Zhou University, Chang Zhou 213003, China;Department of Clinical Chemistry, Institute of Laboratory Medicine, University Hospital of Lund, S-221 85 Lund, Sweden

关键词: Obese;    Diabetes;    Hepatocyte nuclear factor-1α;    Leptin;    Lipoprotein metabolism;    Apolipoprotein M;   

Others  :  1213284
DOI  :  10.1186/1476-511X-3-21

 received in 2004-09-16, accepted in 2004-10-04,  发布年份 2004

【 摘 要 】

Apolipoprotein M (apoM) is a 26-kDa protein that is mainly associated with high-density lipoprotein (HDL) in human plasma, with a small proportion present in triglyceride-rich lipoproteins (TGRLP) and low-density lipoproteins (LDL). Human apoM gene is located in p21.31 on chromosome 6 (chromosome 17, in mouse). Human apoM cDNA (734 base pairs) encodes 188-amino acid residue-long protein. It belongs to lipocalin protein superfamily. Human tissue expression array study indicates that apoM is only expressed in liver and in kidney and small amounts are found in fetal liver and kidney. In situ apoM mRNA hybridization demonstrates that apoM is exclusively expressed in the hepatocytes and in the tubule epithelial cells in kidney. Expression of apoM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF) and leptin in vivo and/or in vitro. It has been demonstrated that apoM expression is dramatically decreased in apoA-I deficient mouse. Hepatocyte nuclear factor-1α (HNF-1α) is an activator of apoM gene promoter. Deficiency of HNF-1α mouse shows lack of apoM expression. Mutations in HNF-1α (MODY3) have reduced serum apoM levels. Expression of apoM is significantly decreased in leptin deficient (ob/ob) mouse or leptin receptor deficient (db/db) mouse. ApoM concentration in plasma is positively correlated to leptin level in obese subjects. These may suggest that apoM is related to the initiation and progression of MODY3 and/or obesity.

【 授权许可】

   
2004 Luo et al; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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