ADIPOQ SNP45 associated with lean body mass in physically active normal weight adolescent girls

• Published in: American journal of human biology 2010-11, Vol.22 (6), p.813-818
• Main Authors: Passariello, Catherine L., Gruodytė, Rita, Hiio, Kelli, Mäestu, Jarek, Jürimäe, Jaak, Saar, Melli, Cicchella, Antonio, Stefanelli, Claudio, Jürimäe, Toivo
• Format: Article
• Language: English
• Subjects: Adiponectin - blood; Adiponectin - genetics; Adolescent; Adolescent Development; Blood Glucose; Body Weights and Measures; Exercise; Female; Genetic Association Studies; Genotype; Humans; Insulin - blood; Polymorphism, Single Nucleotide
• ISSN: 1042-0533; 1520-6300
• DOI: 10.1002/ajhb.21087

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. Objectives 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. Methods 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. Results 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). Conclusions 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.