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G‐2548A Polymorphism of the Leptin Gene Is Correlated with Extreme Obesity in Taiwanese Aborigines
Author(s) -
Wang TsuNai,
Huang MengChuan,
Chang WenTsan,
Ko Albert MinShan,
Tsai EingMei,
Liu ChihShan,
Lee ChienHung,
Ko YingChin
Publication year - 2006
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2006.23
Subject(s) - obesity , leptin , medicine , genotype , leptin receptor , polymorphism (computer science) , endocrinology , biology , genetics , gene
We examined the genetic associations of the G‐2548A polymorphism in the promoter of the leptin ( LEP ) gene and the Gln223Arg (Q223R) polymorphism of the leptin receptor ( LEPR ) gene with obesity. Two hundred twenty‐six obese aboriginal subjects (BMI ≥ 27 kg/m 2 ) and 182 aboriginal subjects with normal weight (BMI < 25 kg/m 2 ) participated in this study. The polymorphisms of LEP G‐2548A and LEPR Q223R were genotyped by polymerase chain reaction/restriction fragment length polymorphism, and their anthropometric characteristics were measured. Levels of leptin, triglycerides, and cholesterol were measured after overnight fasting. We found that the frequencies of the LEP G/G homozygote (22.6%) with Mendelian recessive (χ 2 = 7.89, p = 0.005) and codominant (χ 2 = 7.93, p = 0.02) models to be higher in the extremely obese subjects (BMI ≥ 35 kg/m 2 ) than in normal weight subjects (6.9%) but not in moderately obese subjects (35 > BMI ≥ 27 kg/m 2 ). There was no difference in genotypic frequency of the LEPR Q223R polymorphism between the extreme obese and control groups. We suggest that the LEP −2548 G/G homozygote plays a genetic recessive role in the development of extreme obesity in Taiwanese aborigines.