Dietary fat intake and polymorphisms at the PPARG locus modulate BMI and type 2 diabetes risk in the D.E.S.I.R. prospective study

A. Lamri, Charbel Abi Khalil, R. Jaziri, G. Velho, O. Lantieri, S. Vol, P. Froguel, B. Balkau, M. Marre, F. Fumeron

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Context: Fat-rich diets are involved in many disorders such as obesity and type 2 diabetes (T2D). The Pro12Ala variant of peroxisome proliferator-activated receptor-γ (PPARγ) is known to modulate body mass index (BMI) and T2D risk. Objective: Our aim was to study the interaction effect between PPARγ gene (PPARG) polymorphisms Pro12Ala and 1431C>T and fat intake on incident T2D and BMI in a 9-year prospective cohort drawn from the French general population, the D.E.S.I.R. (Data from an Epidemiological Study on the Insulin Resistance Syndrome) study (n=4676). Methods: Nutritional intake was assessed by a food frequency self-questionnaire completed by each participant. Statistical analyses included logistic regression, analysis of covariance and haplotype analysis, with adjustment for confounding variables. Results: A high fat consumption (the third sex-specific tertile of fat intake, as a percentage of energy intake) was associated with an increased T2D risk among ProPro and CC homozygotes (P interaction = 0.05, odds ratio (OR) (95% confidence interval (95% CI))=1.73 (1.19-2.52) P=0.004 and OR=1.85 (1.27-2.71) P=0.001, respectively) but not in Ala and T carriers. There was a significant interaction effect between Pro12Ala and 1431C>T on BMI (P interaction = 0.004); Ala was associated with lower BMI in CC homozygotes and with higher BMI in T carriers while the opposite was found for ProPro. There was also an interaction effect between Pro12Ala and dietary fat intake on BMI (P interaction = 0.02); AlaAla individuals had a higher BMI than Pro carriers among high fat consumers (27.1 ± 1.0 versus 24.9 ± 0.1 for AlaAla and Pro+, respectively). There was no interaction effect between the 1431C>T single-nucleotide polymorphism and fat intake on BMI. Conclusion: Our results indicate strong genetic and nutritional interaction effects on BMI and T2D risk at the PPARG locus in a general population.

Original languageEnglish
Pages (from-to)218-224
Number of pages7
JournalInternational Journal of Obesity
Volume36
Issue number2
DOIs
Publication statusPublished - Feb 2012
Externally publishedYes

Fingerprint

Peroxisome Proliferator-Activated Receptors
Dietary Fats
Type 2 Diabetes Mellitus
Body Mass Index
Prospective Studies
Fats
Genes
Homozygote
Odds Ratio
Nutrigenomics
Confounding Factors (Epidemiology)
Energy Intake
Haplotypes
Population
Single Nucleotide Polymorphism
Insulin Resistance
Epidemiologic Studies
Obesity
Logistic Models
Regression Analysis

Keywords

  • body mass index
  • fat intake
  • gene-environment interactions
  • genetic variation
  • PPARG
  • type 2 diabetes

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

Dietary fat intake and polymorphisms at the PPARG locus modulate BMI and type 2 diabetes risk in the D.E.S.I.R. prospective study. / Lamri, A.; Abi Khalil, Charbel; Jaziri, R.; Velho, G.; Lantieri, O.; Vol, S.; Froguel, P.; Balkau, B.; Marre, M.; Fumeron, F.

In: International Journal of Obesity, Vol. 36, No. 2, 02.2012, p. 218-224.

Research output: Contribution to journalArticle

Lamri, A. ; Abi Khalil, Charbel ; Jaziri, R. ; Velho, G. ; Lantieri, O. ; Vol, S. ; Froguel, P. ; Balkau, B. ; Marre, M. ; Fumeron, F. / Dietary fat intake and polymorphisms at the PPARG locus modulate BMI and type 2 diabetes risk in the D.E.S.I.R. prospective study. In: International Journal of Obesity. 2012 ; Vol. 36, No. 2. pp. 218-224.
@article{358337a47cc74acf81b847eb88394463,
title = "Dietary fat intake and polymorphisms at the PPARG locus modulate BMI and type 2 diabetes risk in the D.E.S.I.R. prospective study",
abstract = "Context: Fat-rich diets are involved in many disorders such as obesity and type 2 diabetes (T2D). The Pro12Ala variant of peroxisome proliferator-activated receptor-γ (PPARγ) is known to modulate body mass index (BMI) and T2D risk. Objective: Our aim was to study the interaction effect between PPARγ gene (PPARG) polymorphisms Pro12Ala and 1431C>T and fat intake on incident T2D and BMI in a 9-year prospective cohort drawn from the French general population, the D.E.S.I.R. (Data from an Epidemiological Study on the Insulin Resistance Syndrome) study (n=4676). Methods: Nutritional intake was assessed by a food frequency self-questionnaire completed by each participant. Statistical analyses included logistic regression, analysis of covariance and haplotype analysis, with adjustment for confounding variables. Results: A high fat consumption (the third sex-specific tertile of fat intake, as a percentage of energy intake) was associated with an increased T2D risk among ProPro and CC homozygotes (P interaction = 0.05, odds ratio (OR) (95{\%} confidence interval (95{\%} CI))=1.73 (1.19-2.52) P=0.004 and OR=1.85 (1.27-2.71) P=0.001, respectively) but not in Ala and T carriers. There was a significant interaction effect between Pro12Ala and 1431C>T on BMI (P interaction = 0.004); Ala was associated with lower BMI in CC homozygotes and with higher BMI in T carriers while the opposite was found for ProPro. There was also an interaction effect between Pro12Ala and dietary fat intake on BMI (P interaction = 0.02); AlaAla individuals had a higher BMI than Pro carriers among high fat consumers (27.1 ± 1.0 versus 24.9 ± 0.1 for AlaAla and Pro+, respectively). There was no interaction effect between the 1431C>T single-nucleotide polymorphism and fat intake on BMI. Conclusion: Our results indicate strong genetic and nutritional interaction effects on BMI and T2D risk at the PPARG locus in a general population.",
keywords = "body mass index, fat intake, gene-environment interactions, genetic variation, PPARG, type 2 diabetes",
author = "A. Lamri and {Abi Khalil}, Charbel and R. Jaziri and G. Velho and O. Lantieri and S. Vol and P. Froguel and B. Balkau and M. Marre and F. Fumeron",
year = "2012",
month = "2",
doi = "10.1038/ijo.2011.91",
language = "English",
volume = "36",
pages = "218--224",
journal = "International Journal of Obesity",
issn = "0307-0565",
publisher = "Nature Publishing Group",
number = "2",

}

TY - JOUR

T1 - Dietary fat intake and polymorphisms at the PPARG locus modulate BMI and type 2 diabetes risk in the D.E.S.I.R. prospective study

AU - Lamri, A.

AU - Abi Khalil, Charbel

AU - Jaziri, R.

AU - Velho, G.

AU - Lantieri, O.

AU - Vol, S.

AU - Froguel, P.

AU - Balkau, B.

AU - Marre, M.

AU - Fumeron, F.

PY - 2012/2

Y1 - 2012/2

N2 - Context: Fat-rich diets are involved in many disorders such as obesity and type 2 diabetes (T2D). The Pro12Ala variant of peroxisome proliferator-activated receptor-γ (PPARγ) is known to modulate body mass index (BMI) and T2D risk. Objective: Our aim was to study the interaction effect between PPARγ gene (PPARG) polymorphisms Pro12Ala and 1431C>T and fat intake on incident T2D and BMI in a 9-year prospective cohort drawn from the French general population, the D.E.S.I.R. (Data from an Epidemiological Study on the Insulin Resistance Syndrome) study (n=4676). Methods: Nutritional intake was assessed by a food frequency self-questionnaire completed by each participant. Statistical analyses included logistic regression, analysis of covariance and haplotype analysis, with adjustment for confounding variables. Results: A high fat consumption (the third sex-specific tertile of fat intake, as a percentage of energy intake) was associated with an increased T2D risk among ProPro and CC homozygotes (P interaction = 0.05, odds ratio (OR) (95% confidence interval (95% CI))=1.73 (1.19-2.52) P=0.004 and OR=1.85 (1.27-2.71) P=0.001, respectively) but not in Ala and T carriers. There was a significant interaction effect between Pro12Ala and 1431C>T on BMI (P interaction = 0.004); Ala was associated with lower BMI in CC homozygotes and with higher BMI in T carriers while the opposite was found for ProPro. There was also an interaction effect between Pro12Ala and dietary fat intake on BMI (P interaction = 0.02); AlaAla individuals had a higher BMI than Pro carriers among high fat consumers (27.1 ± 1.0 versus 24.9 ± 0.1 for AlaAla and Pro+, respectively). There was no interaction effect between the 1431C>T single-nucleotide polymorphism and fat intake on BMI. Conclusion: Our results indicate strong genetic and nutritional interaction effects on BMI and T2D risk at the PPARG locus in a general population.

AB - Context: Fat-rich diets are involved in many disorders such as obesity and type 2 diabetes (T2D). The Pro12Ala variant of peroxisome proliferator-activated receptor-γ (PPARγ) is known to modulate body mass index (BMI) and T2D risk. Objective: Our aim was to study the interaction effect between PPARγ gene (PPARG) polymorphisms Pro12Ala and 1431C>T and fat intake on incident T2D and BMI in a 9-year prospective cohort drawn from the French general population, the D.E.S.I.R. (Data from an Epidemiological Study on the Insulin Resistance Syndrome) study (n=4676). Methods: Nutritional intake was assessed by a food frequency self-questionnaire completed by each participant. Statistical analyses included logistic regression, analysis of covariance and haplotype analysis, with adjustment for confounding variables. Results: A high fat consumption (the third sex-specific tertile of fat intake, as a percentage of energy intake) was associated with an increased T2D risk among ProPro and CC homozygotes (P interaction = 0.05, odds ratio (OR) (95% confidence interval (95% CI))=1.73 (1.19-2.52) P=0.004 and OR=1.85 (1.27-2.71) P=0.001, respectively) but not in Ala and T carriers. There was a significant interaction effect between Pro12Ala and 1431C>T on BMI (P interaction = 0.004); Ala was associated with lower BMI in CC homozygotes and with higher BMI in T carriers while the opposite was found for ProPro. There was also an interaction effect between Pro12Ala and dietary fat intake on BMI (P interaction = 0.02); AlaAla individuals had a higher BMI than Pro carriers among high fat consumers (27.1 ± 1.0 versus 24.9 ± 0.1 for AlaAla and Pro+, respectively). There was no interaction effect between the 1431C>T single-nucleotide polymorphism and fat intake on BMI. Conclusion: Our results indicate strong genetic and nutritional interaction effects on BMI and T2D risk at the PPARG locus in a general population.

KW - body mass index

KW - fat intake

KW - gene-environment interactions

KW - genetic variation

KW - PPARG

KW - type 2 diabetes

UR - http://www.scopus.com/inward/record.url?scp=84857051628&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84857051628&partnerID=8YFLogxK

U2 - 10.1038/ijo.2011.91

DO - 10.1038/ijo.2011.91

M3 - Article

VL - 36

SP - 218

EP - 224

JO - International Journal of Obesity

JF - International Journal of Obesity

SN - 0307-0565

IS - 2

ER -