Genetic and environmental determinants of the susceptibility of Amerindian derived populations for having hypertriglyceridemia.
Here, we discuss potential explanations for the higher prevalence of hypertriglyceridemia in populations with an Amerindian background. Although environmental factors are the triggers, the search for the ethnic related factors that explain the increased susceptibility of the Amerindians is a promising area for research. The study of the genetics of hypertriglyceridemia in Hispanic populations faces several challenges. Ethnicity could be a major confounding variable to prove genetic associations. Despite that, the study of hypertriglyceridemia in Hispanics has resulted in significant contributions. Two GWAS reports have exclusively included Mexican mestizos. Fifty percent of the associations reported in Caucasians could be generalized to the Mexicans, but in many cases the Mexican lead SNP was different than that reported in Europeans. Both reports included new associations with apo B or triglycerides concentrations. The frequency of susceptibility alleles in Mexicans is higher than that found in Europeans for several of the genes with the greatest effect on triglycerides levels. An example is the SNP rs964184 in APOA5. The same trend was observed for ANGPTL3 and TIMD4 variants. In summary, we postulate that the study of the genetic determinants of hypertriglyceridemia in Amerindian populations which have major changes in their lifestyle, may prove to be a great resource to identify new genes and pathways associated with hypertriglyceridemia.
Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Médicas y Nutrición, México City, México. Electronic address: caguilarsalinas@yahoo.com.
Carlos A
CA
Aguilar-Salinas
Unit of Molecular Biology and Genomic Medicine, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México and Instituto Nacional de Ciencias Médicas y Nutrición, México City, México. Electronic address: mttusie@gmail.com.
Teresa
T
Tusie-Luna
Department of Human Genetics, David Geffen School of Medicine at UCLA, Los Angeles, USA; Molecular Biology Institute at UCLA, Los Angeles, USA. Electronic address: ppajukanta@mednet.ucla.edu.
Päivi
P
Pajukanta
D000091303:Angiopoietin-Like Protein 3; D000075802:Angiopoietin-like Proteins; D042682:Angiopoietins / Q000235:genetics* / Q000378:metabolism; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A / Q000235:genetics* / Q000378:metabolism; D001055:Apolipoproteins B / Q000235:genetics* / Q000378:metabolism; D004198:Disease Susceptibility; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D006630:Hispanic or Latino; D006801:Humans; D006950:Hyperlipidemia, Familial Combined / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D006952:Hyperlipoproteinemia Type III / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D006953:Hyperlipoproteinemia Type IV / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D015228:Hypertriglyceridemia / Q000209:etiology* / Q000235:genetics / Q000378:metabolism; D007197:Indians, Central American; D007198:Indians, North American; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism; D008800:Mexico / Q000208:ethnology; D020412:Multifactorial Inheritance; D011110:Polymorphism, Genetic; D014481:United States
C479896:ANGPTL3 protein, human; C437704:APOA5 protein, human; D000091303:Angiopoietin-Like Protein 3; D000075802:Angiopoietin-like Proteins; D042682:Angiopoietins; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A; D001055:Apolipoproteins B; D008565:Membrane Proteins; C512411:TIMD4 protein, human
Hispanics; Latin America; Triglycerides