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Vitamin D reduces the inflammatory response and restores glucose uptake in adipocytes

Abstract : Scope Obesity is strongly associated with low-grade inflammation, notably due to an overproduction of proinflammatory markers by adipose tissue and adipocytes as well as a vitamin D deficiency. Whether these problems are interrelated has not been clearly established. Methods and results In the present report, decreases in the levels of inflammatory markers such as IL-6, MCP-1, and IL-1 beta (mRNA and protein level) in human adipocytes and in 3T3-L1 adipocytes were observed after 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) treatment. Such treatment also decreased the expression of the TNF-alpha-mediated proinflammatory marker in 3T3-L1 and human adipocytes. A similar effect was observed in adipocyte-macrophage co-culture systems in which 1,25-(OH)2D3 decreased proinflammatory marker expression under basal and TNF-alpha-stimulated conditions. The involvement of VDR and NF-kappa B was confirmed in these regulations. Incubation with 1,25-(OH)2D3 also resulted in the dephosphorylation of p38, which is linked to the transcriptional induction of several Dusp family members. Functional consequences of the 1,25-(OH)2D3 treatment on glucose uptake and AKT phosphorylation were observed. Conclusion The improvement of both proinflammatory status and glucose uptake in adipocytes under 1,25-(OH)2D3 effect suggests that low-grade inflammation could be linked to vitamin D deficiency. This observation offers new perspectives in the context of obesity and associated physiopathological disorders.
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https://hal.inrae.fr/hal-02648214
Déposant : Migration Prodinra <>
Soumis le : vendredi 29 mai 2020 - 09:05:22
Dernière modification le : vendredi 17 juillet 2020 - 15:46:26

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Julie Marcotorchino, Erwan Gouranton, Beatrice Romier, Franck Tourniaire, Julien Astier, et al.. Vitamin D reduces the inflammatory response and restores glucose uptake in adipocytes. Molecular Nutrition and Food Research, Wiley-VCH Verlag, 2012, 56 (12), pp.1771 - 1782. ⟨10.1002/mnfr.201200383⟩. ⟨hal-02648214⟩

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