title: Leptin receptor gene polymorphisms and morbid obesity in Mexican patients.
abstract: BACKGROUND
  Human obesity is due to a complex interaction among environmental, behavioral, developmental and genetic factors, including the interaction of leptin (LEP) and leptin receptor (LEPR). SeveralLEPRmutations and polymorphisms have been described in patients with early onset severe obesity and hyperphagic eating behavior; however, some contradictory findings have also been reported. In the present study we explored the association of sixLEPRgene polymorphisms in patients with morbid obesity.
  
  
  RESULTS
  Twenty eight patients with morbid obesity and 56 non-obese Mexican Mestizo individuals were included. Typing of rs1137100, rs1137101, rs1805134, Ser492Thr, rs1805094 and rs1805096LEPRpolymorphisms was performed by PCR and allele specific hybridization. TheLEPRSer492Thr polymorphism was monomorphic with the presence of only the Ser492Thr-G allele. Allele C and genotype T/C for rs1805134 polymorphism were associated with susceptibility to morbid obesity (p= 0.02 andp= 0.03, respectively). No association was observed with any haplotype. Linkage disequilibrium (LD) showed that five polymorphisms (rs1137100, rs1137101, rs1805134, rs1805094 and rs1805096) were in absolute (D' = 1) but none in perfect (r2= 1) LD.
  
  
  CONCLUSIONS
  Our results suggest that rs1805134 polymorphism could be involved in the development of morbid obesity, whilst none of the alleles of theLEPRgene, rs1137100, rs1137101, rs1805094 and rs1805096 were associated as risk factors. However, more studies are necessary to confirm or reject this hypothesis.
authors.affiliation: Departamento de Cirugia Endoscopica, Hospital General "Dr. Manuel Gea Gonzalez", Mexico City, Mexico.
authors.forename: Martin Edgardo
authors.initials: ME
authors.lastname: Rojano-Rodriguez
authors.affiliation: Departamento de Cirugia Endoscopica, Hospital General "Dr. Manuel Gea Gonzalez", Mexico City, Mexico.
authors.forename: Jose Luis
authors.initials: JL
authors.lastname: Beristain-Hernandez
authors.affiliation: Departamento de Biologia Molecular e Histocompatibilidad, Hospital General "Dr. Manuel Gea Gonzalez", SSA, Calzada de Tlalpan 4800, Col. Seccion XVI, 14080 Mexico City, Mexico.
authors.forename: Beatriz
authors.initials: B
authors.lastname: Zavaleta-Villa
authors.affiliation: Departamento de Ecologia de Agentes Patogenos, Hospital General "Dr. Manuel Gea Gonzalez", Mexico City, Mexico.
authors.forename: Pablo
authors.initials: P
authors.lastname: Maravilla
authors.affiliation: Departamento de Biologia Molecular e Histocompatibilidad, Hospital General "Dr. Manuel Gea Gonzalez", SSA, Calzada de Tlalpan 4800, Col. Seccion XVI, 14080 Mexico City, Mexico.
authors.forename: Mirza
authors.initials: M
authors.lastname: Romero-Valdovinos
authors.affiliation: Departamento de Biologia Molecular e Histocompatibilidad, Hospital General "Dr. Manuel Gea Gonzalez", SSA, Calzada de Tlalpan 4800, Col. Seccion XVI, 14080 Mexico City, Mexico.
authors.forename: Angelica
authors.initials: A
authors.lastname: Olivo-Diaz
mesh_terms: D000328:Adult; D000483:Alleles; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D015810:Linkage Disequilibrium; D008297:Male; D008800:Mexico; D009767:Obesity, Morbid / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D054411:Receptors, Leptin / Q000235:genetics*
chemical_list: D054411:Receptors, Leptin
keywords: Genetic susceptibility; LEPR; Morbid obesity; Single nucleotide polymorphisms