title: Catalase rs769214 SNP in elderly malnutrition and during renutrition: is glucagon to blame?
abstract: Impaired glucose tolerance is common during aging. The transcription factor PAX6 is involved in glucose homeostasis. Computational promoter sequence analysis of the catalase gene highlighted a putative PAX6 binding site on the rs769214 polymorphism A allele. Creation of this binding site has been suggested to explain renutrition inefficiency in malnourished elderly patients. Our aim was to evaluate the link between the rs769214 polymorphism of the catalase gene and glucose homeostasis in malnourished elderly patients at inclusion and during renutrition. Thirty-three malnourished elderly Caucasian inpatients were recruited. Nutritional and inflammatory statuses were assessed and a multiplex adipokine analysis was conducted at inclusion and discharge from the Geriatric Nutritional Care Unit at Charles-Foix Hospital (Ivry-sur-Seine, France). Serum glucagon, PAI-1, and TNF-α levels were significantly lower in the A-allele carriers at inclusion. During renutrition, A-allele carriers exhibited increased serum glucagon, PAI-1, and TNF-α variation. After renutrition, levels of these parameters were similar for A-allele carriers and G-allele carriers. A logistic ordinal multivariate regression analysis linked only variation of glucagon to rs769214 SNP. These results support a role for catalase SNP in the efficiency of renutrition in malnourished elderly patients via the modulation of glucagon secretion, probably involving PAX6.
authors.affiliation: EA4466, Faculty of Pharmacy, Paris Descartes University, Sorbonne Paris Cité 75006 Paris cedex, France.
authors.forename: M
authors.initials: M
authors.lastname: Hebert-Schuster
authors.forename: C H
authors.initials: CH
authors.lastname: Cottart
authors.forename: C
authors.initials: C
authors.lastname: Laguillier-Morizot
authors.forename: A
authors.initials: A
authors.lastname: Raynaud-Simon
authors.forename: J L
authors.initials: JL
authors.lastname: Golmard
authors.forename: L
authors.initials: L
authors.lastname: Cynober
authors.forename: J L
authors.initials: JL
authors.lastname: Beaudeux
authors.forename: E E
authors.initials: EE
authors.lastname: Fabre
authors.forename: V
authors.initials: V
authors.lastname: Nivet-Antoine
mesh_terms: D000368:Aged; D000483:Alleles; D001665:Binding Sites / Q000235:genetics; D054316:Biomarkers, Pharmacological / Q000097:blood; D002374:Catalase / Q000235:genetics / Q000378:metabolism*; D019295:Computational Biology; D004252:DNA Mutational Analysis; D005136:Eye Proteins / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D005934:Glucagon / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D018149:Glucose Intolerance; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D044342:Malnutrition / Q000097:blood / Q000178:diet therapy / Q000235:genetics*; D000071841:PAX6 Transcription Factor; D051761:Paired Box Transcription Factors / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D020641:Polymorphism, Single Nucleotide; D012097:Repressor Proteins / Q000378:metabolism; D015533:Transcriptional Activation; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D054316:Biomarkers, Pharmacological; D005136:Eye Proteins; D018398:Homeodomain Proteins; D000071841:PAX6 Transcription Factor; C000605730:PAX6 protein, human; D051761:Paired Box Transcription Factors; D017395:Plasminogen Activator Inhibitor 1; D012097:Repressor Proteins; D014409:Tumor Necrosis Factor-alpha; D005934:Glucagon; D002374:Catalase