Lys656Asn polymorphism of leptin receptor gene and metabolic syndrome in obese patients
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Updated: May 31, 2026
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Published on: June 3, 2016
D A De Luis1, M Gonzalez Sagrado, R Aller
1Center of Investigation of Endocrinology and Clinical Nutrition, Medicine School and Unit of Investigation, Hospital Universitario Rio Hortega, University of Valladolid, Valladolid, Spain. dadluis@yahoo.es
Background:
The etiology of common obesity is complex, because many genetic, environmental and metabolic factors might act. Alterations of the normal leptin receptor gene be involved in the development of obesity. The polymorphism on codon 656 produces a change in charge, making this change a possibility to be functional.
Objective:
The aim of our study was to investigate the relationship between metabolic syndrome and Lys656Asn polymorphism in obese patients.
Design:
A population of 714 obese patients (body mass index > 30) was analyzed in cross-sectional survey. A bioimpedance, blood pressure, a serial assessment of nutritional intake with 3 days written food records and biochemical analysis were performed.
Results:
Four hundred and seventy eight patients (66.9%) had the genotype Lys656/Lys 656 (wild group), whereas 236 (33.1%) had either the genotype Lys656/Asn656 (212 patients, 29.7%) or the genotype Asn656/Asn656 (24 patients, 3.4%) (mutant group). Prevalence of metabolic syndrome (MS) with ATP III definition was 49.4% (353 patients; 35.1% males and 64.9% females) and 50.6% patients without MS (n = 361; 25.2% males and 75.8% females). Prevalence of leptin receptor (LEPR) genotypes was similar in patients with metabolic syndrome (65.5% wild genotype and 34.5% mutant genotype) and without metabolic syndrome (68.3% wild genotype and 31.7% mutant genotype). No differences in anthropometric and biochemical parameters were detected between genotypes in the same group of metabolic syndrome.
Conclusion:
The finding of our study is the lack of association of the Lys656/Asn656 and Asn656/ Asn656 genotypes with metabolic syndrome.
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