Original Research Article
ADIPOQ SNP45 associated with lean body mass in physically active normal weight adolescent girls
Article first published online: 28 SEP 2010
Copyright © 2010 Wiley-Liss, Inc.
American Journal of Human Biology
Volume 22, Issue 6, pages 813–818, November/December 2010
How to Cite
Passariello, C. L., Gruodytė, R., Hiio, K., Mäestu, J., Jürimäe, J., Saar, M., Cicchella, A., Stefanelli, C. and Jürimäe, T. (2010), ADIPOQ SNP45 associated with lean body mass in physically active normal weight adolescent girls. Am. J. Hum. Biol., 22: 813–818. doi: 10.1002/ajhb.21087
- Issue published online: 16 OCT 2010
- Article first published online: 28 SEP 2010
- Manuscript Accepted: 13 JUL 2010
- Manuscript Revised: 27 MAY 2010
- Manuscript Received: 21 FEB 2010
Recently, two single nucleotide polymorphisms at position 45 and 276 on the adiponectin gene (ADIPOQ) have been recognized as determinants of total adiponectin levels, insulin resistance, and risk for diabetes in various obese populations.
The aim of this study was to determine whether these two polymorphisms are indeed determinants in the development of metabolic disorders or whether they are secondary to other confounding factors.
To do so, we have selected 170 physically active adolescent girls (mean age, 14.03 ± 1.5 years and mean body mass index, 19.98 ± 2.5 kg/m2) devoid of any metabolic diseases or confounding factors, to better attribute any findings to genotype effects. Concentration of adiponectin, insulin, and glucose were determined from blood samples with appropriate kits. Body fat parameters were evaluated with dual-energy X-ray absorptiometry, and genotype was analyzed with DNA extracted from whole blood samples followed by polymerase chain reaction and electrophoresis to separate alleles.
Neither single nucleotide polymorphism +45T/G nor +276G/T was related to homeostasis model assessment index or adiponectin levels; however, the presence of the G allele on site 45 favored a significant decrease in lean body mass compared with those who were T homozygous (TG:36.90/TT:41.07 kg, P < 0.05).
Results suggest that the reported increase in the risk of diabetes in subjects that were G allele carriers at site 45 in obese populations compared with normal-weight populations can be linked instead to a change in muscle mass or the muscle itself present in this genotype group. Am. J. Hum. Biol., 2010. © 2010 Wiley-Liss, Inc.