The common biological basis for common complex diseases: evidence from lipoprotein lipase gene.
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.
Xie
Cui
C
Laboratory of Disorder Genes, School of Public Health, Chongqing University of Medical Sciences, Chongqing 400016, People's Republic of China.
Wang
Zeng Chan
ZC
Liu
Xiao Feng
XF
Yang
Mao Sheng
MS
D000544:Alzheimer Disease / Q000235:genetics; D003327:Coronary Disease / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D004194:Disease / Q000235:genetics*; D050171:Dyslipidemias / Q000235:genetics; D006801:Humans; D006973:Hypertension / Q000235:genetics; D008071:Lipoprotein Lipase / Q000235:genetics* / Q000378:metabolism*; D008954:Models, Biological
D008071:Lipoprotein Lipase