title: Association of biochemical parameters and RAGE gene polymorphisms in healthy infants and their mothers.
abstract: BACKGROUND
  The receptor for advanced glycation end-products (RAGEs) and its gene polymorphisms are implicated in the pathogenesis of different chronic diseases including diabetes and its complications. Infant formulas contain high amounts of advanced glycation end-products (AGEs) - the ligands of RAGE.
  
  
  METHODS
  In this cross-sectional study, we examined the impact of G82S and -374 A/T polymorphisms in the gene encoding RAGE on standard blood chemistry, soluble (s)RAGE and inflammatory markers in 244 healthy infants (3-16months of age) and in 119 healthy mothers. Children were subdivided according to age (younger and older than 8months) and for the -374 A/T polymorphism according to the feeding regimen (breast-fed vs. infant formula-fed).
  
  
  RESULTS
  Minor allele of the RAGE gene polymorphism G82S was associated with reduced plasma sRAGE in all age groups and with increased sICAM-1 in older children and mothers. Minor allele carrying mothers had decreased insulin sensitivity and HDL. The A allele of the RAGE gene promoter polymorphism -374 A/T was associated with higher indices of insulin resistance in young infant formula-fed, but not breast-fed children. In older, formerly infant formula-fed children signs of insulin resistance diminished, while formerly breast-fed children with A allele were more insulin sensitive.
  
  
  CONCLUSIONS
  The phenotype of minor allele carriers in G82S is associated with reduced levels of protective sRAGE in healthy infants. With increasing age sICAM-1 levels increased and insulin resistance developed. In early childhood the phenotype of the -374 A/T polymorphism was diet-dependently associated with changes in glucose metabolism, which diminished with increasing age.
authors.affiliation: Department of Clinical and Experimental Pharmacotherapy, Slovak Medical University, Bratislava, Slovakia. boor@email.cz
authors.forename: P
authors.initials: P
authors.lastname: Boor
authors.forename: P
authors.initials: P
authors.lastname: Celec
authors.forename: K
authors.initials: K
authors.lastname: Klenovicsová
authors.forename: B
authors.initials: B
authors.lastname: Vlková
authors.forename: T
authors.initials: T
authors.lastname: Szemes
authors.forename: G
authors.initials: G
authors.lastname: Minárik
authors.forename: J
authors.initials: J
authors.lastname: Turna
authors.forename: K
authors.initials: K
authors.lastname: Sebeková
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D004032:Diet; D005260:Female; D017127:Glycation End Products, Advanced / Q000097:blood; D006262:Health; D006801:Humans; D007223:Infant; D041943:Infant Formula; D007249:Inflammation / Q000097:blood / Q000378:metabolism; D008297:Male; D008895:Milk, Human; D009035:Mothers; D010641:Phenotype; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000235:genetics*
chemical_list: D001786:Blood Glucose; D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic