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Type A competitiveness traits correlate with downregulation of c-Fos expression in patients with type 1 diabetes

Abstract : Aim Type A personality has been associated with increased survival in people with type 1 diabetes (T1D). Systemic low-grade inflammation may play a critical role, as suggested in recent reports, although the links between the inflammatory circulating transcriptome and Type A remain unknown. This prompted our exploration of the potential associations between Type A personality and c-Fos gene expression, a candidate gene closely linked to inflammatory processes, in T1D. Methods Type A personality was assessed by Bortner questionnaire in patients with T1D, and two subscales – ‘speed’ and ‘competitiveness’ – were used to measure these specific dimensions of Type A. Expression of the c-Fos gene was assessed by a quantitative real-time polymerase chain reaction technique. Results This pilot study included 20 men with T1D. Multivariable analyses showed an independent inverse association between Type A competitiveness score and c-Fos expression, while a regression model adjusted for age, body mass index and HbA1c levels revealed a significant inverse relationship between c-Fos transcripts and Type A competitiveness (P = 0.003). Conclusion This strong association between Type A competitiveness and reduced c-Fos expression is in line with recent data suggesting a psychobiological influence of the Type A profile in T1D via inflammatory pathways. Le texte complet de cet article est disponible en PDF.
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https://hal-univ-bourgogne.archives-ouvertes.fr/hal-01953572
Contributeur : Lnc - Université de Bourgogne <>
Soumis le : jeudi 13 décembre 2018 - 10:22:30
Dernière modification le : jeudi 9 avril 2020 - 11:55:30

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J.-C. Chauvet-Gélinier, A.-L. Mosca-Boidron, C. Lemogne, S. Ragot, N. Forestier, et al.. Type A competitiveness traits correlate with downregulation of c-Fos expression in patients with type 1 diabetes. Journal of Diabetes & Metabolism, OMICS International, In press, ⟨10.1016/j.diabet.2018.11.005⟩. ⟨hal-01953572⟩

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