ACDC/adiponectin polymorphisms are associated with severe childhood and adult obesity

Nabila Bouatia-Naji, David Meyre, Stéphane Lobbens, Karin Séron, Frédéric Fumeron, Beverley Balkau, Barbara Heude, Béatrice Jouret, Philipp E. Scherer, Christian Dina, Jacques Weill, Philippe Froguel

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Abstract

Common single nucleotide polymorphisms (SNPs) in the ACDC adiponectin encoding gene have been associated with insulin resistance and type 2 diabetes in several populations. Here, we investigate the role of SNPs -11,377C>G, -11,391G>A, +45T>G, and +276G>T in 2,579 French Caucasians (1,229 morbidly obese and 1,350 control subjects). We found an association between severe forms of obesity and -11,377C (odds ratio 1.23, P = 0.001) and +276T (1.19, P = 0.006). Surprisingly, alternative alleles -11,377G and +276G have been previously reported as risk factors for type 2 diabetes. Transmission disequilibrium tests showed a trend in overtransmission (56.7%) of a risk haplotype 1(C)-1(G)-1(T)-2(T) including -11,377C and +276T in 634 obesity trios (P = 0.097). Family-based analysis in 400 trios from the general population indicated association between obesity haplotype and higher adiponectin levels, suggesting a role of hyperadiponectinemia in weight gain. However, experiments studying the putative roles of SNPs -11,377C>G and +276G>T on ACDC functionality were not conclusive. In contrast, promoter SNP -11,391G>A was associated with higher adiponectin levels in obese children (P = 0.005) and in children from the general population (0.00007). In vitro transcriptional assays showed that -11,391A may increase ACDC activity. In summary, our study suggests that variations at the ACDC/adiponectin gene are associated with risk of severe forms of obesity. However, the mechanisms underlying these possible associations are not fully understood.

Original languageEnglish (US)
Pages (from-to)545-550
Number of pages6
JournalDiabetes
Volume55
Issue number2
DOIs
StatePublished - Feb 2006

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Morbid Obesity
Pediatric Obesity
Adiponectin
Single Nucleotide Polymorphism
Type 2 Diabetes Mellitus
Haplotypes
Obesity
Population
Genes
Weight Gain
Insulin Resistance
Alleles
Odds Ratio

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Bouatia-Naji, N., Meyre, D., Lobbens, S., Séron, K., Fumeron, F., Balkau, B., ... Froguel, P. (2006). ACDC/adiponectin polymorphisms are associated with severe childhood and adult obesity. Diabetes, 55(2), 545-550. https://doi.org/10.2337/diabetes.55.02.06.db05-0971

ACDC/adiponectin polymorphisms are associated with severe childhood and adult obesity. / Bouatia-Naji, Nabila; Meyre, David; Lobbens, Stéphane; Séron, Karin; Fumeron, Frédéric; Balkau, Beverley; Heude, Barbara; Jouret, Béatrice; Scherer, Philipp E.; Dina, Christian; Weill, Jacques; Froguel, Philippe.

In: Diabetes, Vol. 55, No. 2, 02.2006, p. 545-550.

Research output: Contribution to journalArticle

Bouatia-Naji, N, Meyre, D, Lobbens, S, Séron, K, Fumeron, F, Balkau, B, Heude, B, Jouret, B, Scherer, PE, Dina, C, Weill, J & Froguel, P 2006, 'ACDC/adiponectin polymorphisms are associated with severe childhood and adult obesity', Diabetes, vol. 55, no. 2, pp. 545-550. https://doi.org/10.2337/diabetes.55.02.06.db05-0971
Bouatia-Naji N, Meyre D, Lobbens S, Séron K, Fumeron F, Balkau B et al. ACDC/adiponectin polymorphisms are associated with severe childhood and adult obesity. Diabetes. 2006 Feb;55(2):545-550. https://doi.org/10.2337/diabetes.55.02.06.db05-0971
Bouatia-Naji, Nabila ; Meyre, David ; Lobbens, Stéphane ; Séron, Karin ; Fumeron, Frédéric ; Balkau, Beverley ; Heude, Barbara ; Jouret, Béatrice ; Scherer, Philipp E. ; Dina, Christian ; Weill, Jacques ; Froguel, Philippe. / ACDC/adiponectin polymorphisms are associated with severe childhood and adult obesity. In: Diabetes. 2006 ; Vol. 55, No. 2. pp. 545-550.
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abstract = "Common single nucleotide polymorphisms (SNPs) in the ACDC adiponectin encoding gene have been associated with insulin resistance and type 2 diabetes in several populations. Here, we investigate the role of SNPs -11,377C>G, -11,391G>A, +45T>G, and +276G>T in 2,579 French Caucasians (1,229 morbidly obese and 1,350 control subjects). We found an association between severe forms of obesity and -11,377C (odds ratio 1.23, P = 0.001) and +276T (1.19, P = 0.006). Surprisingly, alternative alleles -11,377G and +276G have been previously reported as risk factors for type 2 diabetes. Transmission disequilibrium tests showed a trend in overtransmission (56.7{\%}) of a risk haplotype 1(C)-1(G)-1(T)-2(T) including -11,377C and +276T in 634 obesity trios (P = 0.097). Family-based analysis in 400 trios from the general population indicated association between obesity haplotype and higher adiponectin levels, suggesting a role of hyperadiponectinemia in weight gain. However, experiments studying the putative roles of SNPs -11,377C>G and +276G>T on ACDC functionality were not conclusive. In contrast, promoter SNP -11,391G>A was associated with higher adiponectin levels in obese children (P = 0.005) and in children from the general population (0.00007). In vitro transcriptional assays showed that -11,391A may increase ACDC activity. In summary, our study suggests that variations at the ACDC/adiponectin gene are associated with risk of severe forms of obesity. However, the mechanisms underlying these possible associations are not fully understood.",
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AU - Bouatia-Naji, Nabila

AU - Meyre, David

AU - Lobbens, Stéphane

AU - Séron, Karin

AU - Fumeron, Frédéric

AU - Balkau, Beverley

AU - Heude, Barbara

AU - Jouret, Béatrice

AU - Scherer, Philipp E.

AU - Dina, Christian

AU - Weill, Jacques

AU - Froguel, Philippe

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N2 - Common single nucleotide polymorphisms (SNPs) in the ACDC adiponectin encoding gene have been associated with insulin resistance and type 2 diabetes in several populations. Here, we investigate the role of SNPs -11,377C>G, -11,391G>A, +45T>G, and +276G>T in 2,579 French Caucasians (1,229 morbidly obese and 1,350 control subjects). We found an association between severe forms of obesity and -11,377C (odds ratio 1.23, P = 0.001) and +276T (1.19, P = 0.006). Surprisingly, alternative alleles -11,377G and +276G have been previously reported as risk factors for type 2 diabetes. Transmission disequilibrium tests showed a trend in overtransmission (56.7%) of a risk haplotype 1(C)-1(G)-1(T)-2(T) including -11,377C and +276T in 634 obesity trios (P = 0.097). Family-based analysis in 400 trios from the general population indicated association between obesity haplotype and higher adiponectin levels, suggesting a role of hyperadiponectinemia in weight gain. However, experiments studying the putative roles of SNPs -11,377C>G and +276G>T on ACDC functionality were not conclusive. In contrast, promoter SNP -11,391G>A was associated with higher adiponectin levels in obese children (P = 0.005) and in children from the general population (0.00007). In vitro transcriptional assays showed that -11,391A may increase ACDC activity. In summary, our study suggests that variations at the ACDC/adiponectin gene are associated with risk of severe forms of obesity. However, the mechanisms underlying these possible associations are not fully understood.

AB - Common single nucleotide polymorphisms (SNPs) in the ACDC adiponectin encoding gene have been associated with insulin resistance and type 2 diabetes in several populations. Here, we investigate the role of SNPs -11,377C>G, -11,391G>A, +45T>G, and +276G>T in 2,579 French Caucasians (1,229 morbidly obese and 1,350 control subjects). We found an association between severe forms of obesity and -11,377C (odds ratio 1.23, P = 0.001) and +276T (1.19, P = 0.006). Surprisingly, alternative alleles -11,377G and +276G have been previously reported as risk factors for type 2 diabetes. Transmission disequilibrium tests showed a trend in overtransmission (56.7%) of a risk haplotype 1(C)-1(G)-1(T)-2(T) including -11,377C and +276T in 634 obesity trios (P = 0.097). Family-based analysis in 400 trios from the general population indicated association between obesity haplotype and higher adiponectin levels, suggesting a role of hyperadiponectinemia in weight gain. However, experiments studying the putative roles of SNPs -11,377C>G and +276G>T on ACDC functionality were not conclusive. In contrast, promoter SNP -11,391G>A was associated with higher adiponectin levels in obese children (P = 0.005) and in children from the general population (0.00007). In vitro transcriptional assays showed that -11,391A may increase ACDC activity. In summary, our study suggests that variations at the ACDC/adiponectin gene are associated with risk of severe forms of obesity. However, the mechanisms underlying these possible associations are not fully understood.

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