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Association of PPAR ‐γ gene polymorphisms with obesity and obesity‐associated phenotypes in north indian population
Author(s) -
Prakash Jai,
Srivastava Neena,
Awasthi Shally,
Agarwal C.,
Natu S.,
Rajpal Naresh,
Mittal Balraj
Publication year - 2012
Publication title -
american journal of human biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.559
H-Index - 81
eISSN - 1520-6300
pISSN - 1042-0533
DOI - 10.1002/ajhb.22245
Subject(s) - obesity , adiponectin , medicine , peroxisome proliferator activated receptor , genotype , endocrinology , insulin resistance , biology , phenotype , population , haplotype , polymorphism (computer science) , genetics , gene , environmental health
Objectives: The worldwide increasing prevalence of obesity is considered as a major health problem. Peroxisome proliferator‐activated receptor gamma ( PPAR‐γ ) controls adipocyte differentiation and regulates a number of genes associated with energy homeostasis. In this study, we investigated the association of PPAR‐γ gene Pro12Ala (rs1801282) and C1431T (rs3856806) polymorphisms with morbid obesity and related phenotypes, in north Indian population. Methods: A total of 6,42 subjects, 309, obese and 333 nonobese individuals were included in this case–control study. Insulin, adiponectin, glucose, and lipid levels were estimated using standard protocols. All subjects were genotyped by PCR restriction fragment length polymorphism (PCR‐RFLP) method. Results: The ProAla+AlaAla genotypes of PPAR‐γ Pro12Ala were significantly associated with higher risk of obesity while C1431T polymorphism did not show any significant association. None of the haplotypes showed association with morbid obesity. However, a strong association of variant genotypes was observed with higher levels of insulin, HOMA‐IR, and lower serum adiponectin concentrations. Conclusion: PPAR‐γ gene polymorphisms influence obesity and obesity phenotype in a complex manner, probably involving insulin resistance in north Indian population. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.