Interaction Between PPARγ2 Variants and Gender on the Modulation of Body Weight

Authors

  • Eleonora Morini,

    1. CSS-Mendel Institute, Rome, Italy
    2. Department of Clinical Sciences, Sapienza University, Rome, Italy
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  • Vittorio Tassi,

    1. Research Unit of Diabetes and Endocrine Diseases, CSS Scientific Institute, San Giovanni Rotondo, Italy
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  • Daria Capponi,

    1. CSS-Mendel Institute, Rome, Italy
    2. Department of Clinical Sciences, Sapienza University, Rome, Italy
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  • Ornella Ludovico,

    1. Unit of Endocrinology, CSS Scientific Institute, San Giovanni Rotondo, Italy
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  • Bruno Dallapiccola,

    1. CSS-Mendel Institute, Rome, Italy
    2. Department of Experimental Medicine and Pathology, Sapienza University, Rome, Italy
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  • Vincenzo Trischitta,

    Corresponding author
    1. CSS-Mendel Institute, Rome, Italy
    2. Department of Clinical Sciences, Sapienza University, Rome, Italy
    3. Research Unit of Diabetes and Endocrine Diseases, CSS Scientific Institute, San Giovanni Rotondo, Italy
    4. Unit of Endocrinology, CSS Scientific Institute, San Giovanni Rotondo, Italy
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  • Sabrina Prudente

    Corresponding author
    1. CSS-Mendel Institute, Rome, Italy
    2. Research Unit of Diabetes and Endocrine Diseases, CSS Scientific Institute, San Giovanni Rotondo, Italy
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(s.prudente@css-mendel.it)

(vincenzo.trischitta@uniroma1.it)

Abstract

Conflicting results have been reported regarding the effect of the peroxisome proliferator-activated receptor-γ−2 (PPARγ2) Pro12Ala polymorphism, (singly or in combination with the silent C1431T polymorphism) on BMI. Gender-based dimorphism has been evidenced for genes that affect BMI, but few and conflicting data are available regarding PPARγ2. We sought to investigate whether the Pro12Ala interacts with gender in modulating BMI in 566 nondiabetic unrelated white subjects (men:women = 211:355, age 36.59 ± 11.85; BMI 25.36 ± 4.53). In the whole study population, BMI, fasting glucose and insulin levels, and lipid profile were similar in Ala12 carriers (i.e., XA) and Pro/Pro homozygous subjects. Among the men, but not among the women, X/Ala individuals showed higher BMI (25.9 ± 3.6 vs. 28.2 ± 4.9, P = 0.006) and risk of obesity (odds ratio = 2.85, 95% confidence interval = 1.07–7.62). A significant gene-gender interaction in modulating BMI was observed (P = 0.039). Among the men, but not among the women, those carrying Ala-T haplotype (i.e., containing both Ala12 and T1431 variants) showed the highest BMI (haplo-score = 3.72, P = 0.0014). Our data indicate that in whites from Italy the PPARγ2 Pro12Ala polymorphism interacts with gender in modulating BMI, thereby replicating some, but not all, earlier data obtained in different populations. Whether the PPARγ2-gender interaction is a general phenomenon across different populations, is still an open question, the answer to which requires additional, specifically designed, studies.

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