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.

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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: jalfmtz@unav.es

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