Horm Metab Res 2009; 41(1): 55-61
DOI: 10.1055/s-0028-1087204
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

The − 11391 G/A Polymorphism of the Adiponectin Gene Promoter is Associated with Metabolic Syndrome Traits and the Outcome of an Energy-restricted Diet in Obese Subjects

E. Goyenechea 1 , L. J. Collins 2 , D. Parra 1 , I. Abete 1 , A. B. Crujeiras 1 , S. D. O’Dell 2 , J. A. Martínez 1
  • 1Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona, Spain
  • 2Nutritional Sciences Division, King's College, London, United Kingdom
Further Information

Publication History

received 23.04.2008

accepted 15.07.2008

Publication Date:
23 October 2008 (online)

Abstract

Adiponectin is an adipose tissue–specific hormone that is commonly decreased in obese subjects. Furthermore, single-nucleotide polymorphisms (SNPs) of the adiponectin gene have been associated with metabolic phenotypes. The present study investigated whether the adiponectin gene promoter variant −11391 G/A (rs17300539) could predict the risk of developing traits characterizing the metabolic syndrome (MetS) and the impact of weight management. The −11391 G/A SNP was genotyped in 180 Spanish volunteers (BMI: 31.4±3.2 kg/m2; age: 35±5 years). Clinical measurements were determined at baseline, following an 8-week low-calorie diet (LCD), and at 32 and 60 weeks. At baseline, the GG genotype was associated with higher HOMA-IR, insulin and triacylglyceride concentrations than other genotypes (p<0.05) and was also related with a higher risk of insulin resistance (OR: 2.437, p=0.025) and MetS clinical manifestations (OR: 3.236, p=0.003). Following the LCD, the increased risk in GG subjects compared with others disappeared (p>0.05). By 32 weeks after dietary therapy (n=84), GG carriers had recovered the risk of metabolic comorbidities (OR: 2.420, p=0.043). This risk was even more evident after 60 weeks (OR: 2.875, p=0.014). These data show an increased risk of insulin resistance and MetS complications in obese subjects of the −11391 GG genotype. The risk was markedly reduced during an energy-restricted diet, but was not sustained. Carriage of the A allele therefore confers protection from weight regain, and the effect is particularly evident 32–60 weeks after the dietary intervention, when improvement in GG subjects had disappeared.

References

Correspondence

Prof. J. A. Martínez

Department of Nutrition and Food Sciences, Physiology and Toxicology

University of Navarra

Irunlarrea 1

31008 Pamplona

Spain

Phone: +34/9484/256 00

Fax: +34/9484/256 49

Email: [email protected]