title: Triglyceride level affecting shared susceptibility genes in metabolic syndrome and coronary artery disease.
abstract: Metabolic syndrome is characterized primarily by abdominal obesity, high triglyceride- and low HDL cholesterol levels, elevated blood pressure, and increased fasting glucose levels, which are often associated with coronary heart diseases. Several factors, such as physical inactivity, age, and several endocrine and genetic factors can increase the risk of the development of the disease. Gathered evidence shows, that metabolic syndrome is not only a risk factor for cardiovascular disease, but often both of them have the same shared susceptibility genes, as several genetic variants have shown a predisposition to both diseases. Due to the spread of robust genome wide association studies, the number of candidate genes in metabolic syndrome and coronary heart disease susceptibility increases very rapidly. From the growing spectrum of the genes influencing lipid metabolism (like the LPL; PPARA; APOE; APOAI/CIII/AIV genecluster and APOAS5), the current review focuses on shared susceptibility variants involved in triglyceride metabolism and consequently the effects on the circulating triglyceride levels. As the elevated levels of triglycerides can be associated with disease phenotypes, some of these SNPs can have susceptibility features in both metabolic syndrome and in coronary heart disease, thereby some of them can even represent a kind of susceptibility link between metabolic syndrome and coronary artery disease.
authors.affiliation: University of Pécs, Department of Medical Genetics, Pécs, Hungary.
authors.forename: P
authors.initials: P
authors.lastname: Kisfali
authors.forename: N
authors.initials: N
authors.lastname: Polgár
authors.forename: E
authors.initials: E
authors.lastname: Sáfrány
authors.forename: K
authors.initials: K
authors.lastname: Sümegi
authors.forename: B I
authors.initials: BI
authors.lastname: Melegh
authors.forename: J
authors.initials: J
authors.lastname: Bene
authors.forename: A
authors.initials: A
authors.lastname: Wéber
authors.forename: K
authors.initials: K
authors.lastname: Hetyésy
authors.forename: B
authors.initials: B
authors.lastname: Melegh
mesh_terms: D001053:Apolipoproteins / Q000235:genetics; D003324:Coronary Artery Disease / Q000150:complications / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D006801:Humans; D008071:Lipoprotein Lipase / Q000235:genetics; D024821:Metabolic Syndrome / Q000150:complications / Q000235:genetics*; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D014280:Triglycerides / Q000097:blood* / Q000378:metabolism
chemical_list: D001053:Apolipoproteins; D047492:Peroxisome Proliferator-Activated Receptors; D014280:Triglycerides; D008071:Lipoprotein Lipase