Abstract
The lipoprotein lipase (LPL) gene encodes a rate-limiting enzyme protein that has a key role in the hydrolysis of triglycerides. Hypertriglyceridemia, one widely prevalent syndrome of LPL deficiency and dysfunction, may be a risk factor in the development of dyslipidemia, type II diabetes (T2D), essential hypertension (EH), coronary heart disease (CHD) and Alzheimer's disease (AD). Findings from earlier studies indicate that LPL may have a role in the pathology of these diseases and therefore is a common or shared biological basis for these common complex diseases. To examine this hypothesis, we reviewed articles on the molecular structure, expression and function of the LPL gene, and its potential role in the etiology of diseases. Evidence from these studies indicate that LPL dysfunction is involved in dyslipidemia, T2D, EH, CHD and AD; and support the hypothesis that there is a common or shared biological basis for these common complex diseases.
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Acknowledgements
We are grateful to Professor Michael Gill and Dr Derek Morris from Trinity College Dublin and anonymous peer reviewers for their valuable comments to the revision of this article. This work was partly supported by grants from Chongqing Medical University (No. 0124418029 and No. XBZD200701), the Natural Science Foundation Project of CQ CSTC (No. 2008BB5074) and The Program for Excellent Talents of University in Chongqing Municipality.
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Xie, C., Wang, Z., Liu, X. et al. The common biological basis for common complex diseases: evidence from lipoprotein lipase gene. Eur J Hum Genet 18, 3–7 (2010). https://doi.org/10.1038/ejhg.2009.134
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DOI: https://doi.org/10.1038/ejhg.2009.134
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