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Review
. 2017 Nov 30:6:2073.
doi: 10.12688/f1000research.12938.2. eCollection 2017.

Dyslipidemia: Genetics, lipoprotein lipase and HindIII polymorphism

Affiliations
Review

Dyslipidemia: Genetics, lipoprotein lipase and HindIII polymorphism

Marcos Palacio Rojas et al. F1000Res. .

Abstract

The direct link between lipid metabolism alterations and the increase of cardiovascular risk are well documented. Dyslipidemias, including isolated high LDL-c or mixed dyslipidemia, such as those seen in diabetes (hypertriglyceridemia, high LDL-c or low HDL-c), correlate with a significant risk of cardiovascular and cerebrovascular disease worldwide. This review analyzes the current knowledge concerning the genetic basis of lipid metabolism alterations, emphasizing lipoprotein lipase gene mutations and the HindIII polymorphism, which are associated with decreased levels of triglycerides and LDL-c, as well as higher levels of HDL-c. These patterns would be associated with decreased global morbidity and mortality, providing protection against cardiovascular and cerebrovascular diseases.

Keywords: Dyslipidemia; HindIII; Lipoprotein Lipase; Polymorphisms; coronary artery disease.

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Conflict of interest statement

No competing interests were disclosed.

Figures

Figure 1.
Figure 1.. Chromosomal origin of the LPL gene.
The authors confirm that this is an original image and has not been re-used or adapted from another source.
Figure 2.
Figure 2.. Recognition sequence of HindIII enzyme.
The authors confirm that this is an original image and has not been re-used or adapted from another source.
Figure 3.
Figure 3.. Intron 8, restriction site of HindIII (AAGC TT > AAGC GT).
The authors confirm that this is an original image and has not been re-used or adapted from another source.
Figure 4.
Figure 4.. Enzymatic restriction sites in HindIII .
The authors confirm that this is an original image and has not been re-used or adapted from another source.

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