Apolipoprotein M

被引：49

作者：

Luo G. ^{[1
,2
]}

Zhang X. ^{[2
]}

Nilsson-Ehle P. ^{[1
]}

Xu N. ^{[1
]}

机构：

[1] Department of Clinical Chemistry, Institute of Laboratory Medicine, University Hospital of Lund

[2] Laboratory of Molecular Medicine, Third Affiliated Hospital, Su Zhou University

来源：

Lipids in Health and Disease | / 3卷 / 1期

关键词：

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

D O I：

10.1186/1476-511X-3-21

中图分类号：

学科分类号：

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-1́ (HNF-1́) is an activator of apoM gene promoter. Deficiency of HNF-1́ mouse shows lack of apoM expression. Mutations in HNF-1́ (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. © 2004 Luo et al; licensee BioMed Central Ltd.

引用

共 31 条

[21]

Liang C.P., Tall A.R., Transcriptional profiling reveals global defects in energy metabolism, lipoprotein, and bile acid synthesis and transport with reversal by leptin treatment in ob/ob mouse liver, J Biol Chem, 276, pp. 49066-49076, (2001)

[22]

Xu N., Nilsson-Ehle P., Hurtig M., Ahren B., Both leptin and leptin-receptor are essential for apolipoprotein M expression in vivo, Biochem Biophys Res Commun, 321, pp. 916-921, (2004)

[23]

Xu N., Ahren B., Nilsson-Ehle P., Correlation of Apolipoprotein M with Leptin and Cholesterol in Normal and Obese Subjects, J Nutri Biochem, (2004)

[24]

Bertram L., Tanzi R.E., Alzheimer's disease: One disorder, too many genes?, Hum Mol Genet, 13 SPEC NO 1, (2004)

[25]

Poirier J., Apolipoprotein E and Alzheimer's disease. A role in amyloid catabolism, Ann N Y Acad Sci, 924, pp. 81-90, (2000)

[26]

Strittmatter W.J., Apolipoprotein E and Alzheimer's disease: Signal transduction mechanisms, Biochem Soc Symp, pp. 101-109, (2001)

[27]

Yanagisawa K., Cholesterol and pathological processes in Alzheimer's disease, J Neurosci Res, 70, pp. 361-366, (2002)

[28]

Austen B., Christodoulou G., Terry J.E., Relation between cholesterol levels, statins and Alzheimer's disease in the human population, J Nutr Health Aging, 6, pp. 377-382, (2002)

[29]

Holtzman D.M., Fagan A.M., Potential Role of apoE in Structural Plasticity in the Nervous System

[30]

Implications for Disorders of the Central Nervous System, Trends Cardiovasc Med, 8, pp. 250-255, (1998)

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