OBJECTIVES: The aim of this study was to examine the association of the G-2548A polymorphism of the human leptin gene (LEP) with body mass index (BMI), plasma leptin, insulin, and lipid parameters in a sample of Tunisian population. DESIGN AND METHODS: Two hundred and twenty nine obese patients (BMI>or=30 kg/m(2)) were screened and compared to 251 normal weight subjects (BMI<25 kg/m(2)). The human leptin gene promoter G-2548A genotype was determined by polymerase chain reaction followed by a digestion with the restriction of endonuclease CfoI. RESULTS: In the entire study sample, carriers of -2548A allele had significantly lower leptin levels than homozygous for -2548G allele (14.28+/-9.10 ng/mL vs. 18.27+/-12 ng/mL, p<0.001 respectively) adjusted for BMI and gender. In obese patients but not control, subjects carrying the -2548A allele exhibited lower leptin levels than those with GG genotype (16.96+/-8.27 ng/mL vs. 21.37+/-11.72 ng/mL, p=0.001 respectively) adjusted for BMI and gender. In this group, carriership of the -2548A allele was identified, by multiple linear regression models, as significant independent predictor for leptin levels variability. Separate analyses by gender revealed that only in obese women, the -2548A allele was found to be associated with lower leptin levels independently of BMI (p=0.004). CONCLUSIONS: The present study showed that G-2548A LEP polymorphism is associated with lower leptin levels in Tunisian obese women.
OBJECTIVES: The aim of this study was to examine the association of the G-2548A polymorphism of the humanleptin gene (LEP) with body mass index (BMI), plasma leptin, insulin, and lipid parameters in a sample of Tunisian population. DESIGN AND METHODS: Two hundred and twenty nine obesepatients (BMI>or=30 kg/m(2)) were screened and compared to 251 normal weight subjects (BMI<25 kg/m(2)). The humanleptin gene promoter G-2548A genotype was determined by polymerase chain reaction followed by a digestion with the restriction of endonuclease CfoI. RESULTS: In the entire study sample, carriers of -2548A allele had significantly lower leptin levels than homozygous for -2548G allele (14.28+/-9.10 ng/mL vs. 18.27+/-12 ng/mL, p<0.001 respectively) adjusted for BMI and gender. In obesepatients but not control, subjects carrying the -2548A allele exhibited lower leptin levels than those with GG genotype (16.96+/-8.27 ng/mL vs. 21.37+/-11.72 ng/mL, p=0.001 respectively) adjusted for BMI and gender. In this group, carriership of the -2548A allele was identified, by multiple linear regression models, as significant independent predictor for leptin levels variability. Separate analyses by gender revealed that only in obesewomen, the -2548A allele was found to be associated with lower leptin levels independently of BMI (p=0.004). CONCLUSIONS: The present study showed that G-2548ALEP polymorphism is associated with lower leptin levels in Tunisian obesewomen.
Authors: Shruti Dasgupta; Mohammed Salman; Lokesh B Siddalingaiah; G L Lakshmi; D Xaviour; Jwalapuram Sreenath Journal: Adipocyte Date: 2014-12-20 Impact factor: 4.534
Authors: Mitra Yousefi; Wilfried Karmaus; Hongmei Zhang; Susan Ewart; Hasan Arshad; John W Holloway Journal: Int J Mol Epidemiol Genet Date: 2013-06-25
Authors: Benjamin P Fairfax; Fredrik O Vannberg; Jayachandran Radhakrishnan; Hakon Hakonarson; Brendan J Keating; Adrian V S Hill; Julian C Knight Journal: Hum Mol Genet Date: 2009-11-26 Impact factor: 6.150