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Nutrient-Gene Interactions

Human Galanin (GAL) and Galanin 1 Receptor (GALR1) Variations Are Not Involved in Fat Intake and Early Onset Obesity^1,2

Nadine Schäuble^*,||, Kathrin Reichwald^,||, Wolfgang Grassl^*,**, Helen Bechstein^*, Hans-Christian Müller^*, André Scherag, Frank Geller, Michael Utting, Wolfgang Siegfried, Hanspeter Goldschmidt, John Blundell^#, Clare Lawton^#, Rahul Alam^#, Stephen Whybrow^¶, James Stubbs^¶, Matthias Platzer, Johannes Hebebrand^|| and Anke Hinney^||,3

^* Clinical Research Group, Department of Child and Adolescent Psychiatry, Philipps-University of Marburg, Germany; Genome Analysis, Institute of Molecular Biotechnology (IMB), Jena, Germany; ^** Clinic and Department of Outpatients for Radiology and Nuclear Medicine, Campus, Benjamin Franklin, Charité University Medicine, Berlin, Germany; Institute of Medical Biometry and Epidemiology, Philipps-University of Marburg, Germany; Obesity Treatment Center Insula, Berchtesgaden, Germany; Spessart Klinik, Bad Orb, Germany; ^# Institute of Psychological Sciences, University of Leeds, Leeds, UK; ^¶ The Rowett Research Institute, Bucksburn, Aberdeen, Scotland, UK; ^|| Rheinische Kliniken Essen, Child and Adolescent Psychiatry, University of Duisburg-Essen, Essen, Germany

³To whom correspondence should be addressed. E-mail: Anke.Hinney{at}uni-duisburg-essen.de.

The neuropeptide galanin (GAL) is involved in food intake and in fat ingestion. Presumably, these effects are conveyed via the galanin 1 receptor (GALR1). We screened the coding region of GAL (including 444 bp of its promoter region) and GALR1 for mutations using single-strand conformation polymorphism analysis and denaturing HPLC in up to 191 obese children and adolescents and 106 healthy underweight young adults (students). In GAL, we identified 3 novel single nucleotide polymorphisms (SNPs; silent: g.–419TC, g.–244GA; missense: g.47CT: Ala16Val) and one infrequent missense variation (c.253AG: Asn85Asp), and in GALR1 2 novel SNPs (silent: c.150CT, missense: c.793AT: Ile265Phe). To test for an association with obesity, we genotyped 7 SNPs (GAL: g.–244GA, g.47CT, rs7101947, rs1042577, rs3136540; GALR1: c.150CT, c.793AT) in up to 322 obese children and adolescents compared with up to 277 healthy underweight and normal weight young adults. Furthermore, we analyzed these SNPs with respect to potential effects on the percentage of energy consumed as fat in obese children and adolescents. Allele and genotype frequencies did not differ among the groups tested. In addition, we performed a pedigree transmission disequilibrium test (PDT) for one SNP (GAL: g.–244GA) in 610 (518 independent) obesity-trios (obese child or adolescent and both of its parents). However, the PDT for SNP GAL g.–244GA revealed no transmission disequilibrium. We conclude that the analyzed SNPs in GAL and GALR1 do not play a major role in early onset obesity or dietary fat intake in the obese children and adolescents of our study groups.

KEY WORDS: • percentage fat intake • body weight • adolescents • association

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