Open AccessRole of peroxisome proliferator-activated receptors gene polymorphisms in type 2 diabetes and metabolic syndrome
Author(s) -
Chen Dong,
Hui Zhou,
Chong Shen,
Yu Li,
Yi Ding,
Yonghong Zhang,
Zhirong Guo
Publication year - 2015
Publication title -
world journal of diabetes
Language(s) - English
Resource type - Journals
ISSN - 1948-9358
DOI - 10.4239/wjd.v6.i4.654
Subject(s) - peroxisome proliferator activated receptor , metabolic syndrome , nuclear receptor , endocrinology , lipid metabolism , medicine , peroxisome proliferator activated receptor alpha , receptor , type 2 diabetes , insulin resistance , population , biology , type 2 diabetes mellitus , transcription factor , bioinformatics , diabetes mellitus , genetics , gene , environmental health
Metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) are the serious public health problems worldwide. Moreover, it is estimated that MetS patients have about five-fold greater risk of the T2DM development compared with people without the syndrome. Peroxisome proliferator-activated receptors are a subgroup of the nuclear hormone receptor superfamily of ligand-activated transcription factors which play an important role in the pathogenesis of MetS and T2DM. All three members of the peroxisome proliferator-activated receptor (PPAR) nuclear receptor subfamily, PPARα, PPARβ/δ and PPARγ are critical in regulating insulin sensitivity, adipogenesis, lipid metabolism, and blood pressure. Recently, more and more studies indicated that the gene polymorphism of PPARs, such as Leu(162)Val and Val(227)Ala of PPARα, +294T > C of PPARβ/δ, Pro(12)Ala and C1431T of PPARγ, are significantly associated with the onset and progressing of MetS and T2DM in different population worldwide. Furthermore, a large body of evidence demonstrated that the glucose metabolism and lipid metabolism were influenced by gene-gene interaction among PPARs genes. However, given the complexity pathogenesis of metabolic disease, it is unlikely that genetic variation of a single locus would provide an adequate explanation of inter-individual differences which results in diverse clinical syndromes. Thus, gene-gene interactions and gene-environment interactions associated with T2DM and MetS need future comprehensive studies.