In:
Lifestyle Genomics, S. Karger AG, Vol. 7, No. 4-6 ( 2014), p. 225-231
Abstract:
〈 b 〉 〈 i 〉 Background/Aim: 〈 /i 〉 〈 /b 〉 We studied the molecular pathogenesis of obesity, involving complex interactions between environmental and genetic factors, with a focus on the leptin gene. It was our aim to characterize the LEP -2548G 〉 A leptin polymorphism and lipid profile in obese and normal-weight individuals. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 A total of 212 individuals were divided into the study group including 136 obese patients (body mass index, BMI ≥30) and the control group with 76 normal-weight individuals (BMI 〉 18.5 and ≤24.9). DNA was amplified by polymerase chain reaction and restriction fragment length polymorphism. The lipid profile was analyzed by enzymatic colorimetric methods. The level of significance was set at p 〈 0.05. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 There was a prevalence of the GA genotype in both groups. However, comparative group analysis showed an association of the recessive model (AA+GA) with increased triglycerides (TG) and decreased high-density lipoprotein cholesterol (HDL-C) levels in the study group. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 This study did not confirm an association between obesity and the LEP -2548G 〉 A polymorphism. However, AA+GA genotypes, in the presence of obesity, seem to contribute to a reduction in HDL-C and an increase in TG compared with normal-weight individuals. This should be confirmed in further studies.
Type of Medium:
Online Resource
ISSN:
2504-3161
,
2504-3188
Language:
English
Publisher:
S. Karger AG
Publication Date:
2014
detail.hit.zdb_id:
2908437-4
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