Study Title:
Vitamin D reduces the inflammatory response and restores glucose uptake in adipocytes.
Study 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-1β (mRNA and protein level) in human adipocytes and in 3T3-L1 adipocytes were observed after 1,25-dihydroxyvitamin D3 (1,25-(OH)(2) D(3) ) treatment. Such treatment also decreased the expression of the TNF-α-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)(2) D(3) decreased proinflammatory marker expression under basal and TNF-α-stimulated conditions. The involvement of VDR and NF-κB was confirmed in these regulations. Incubation with 1,25-(OH)(2) D(3) 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)(2) D(3) 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)(2) D(3) 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.
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-1β (mRNA and protein level) in human adipocytes and in 3T3-L1 adipocytes were observed after 1,25-dihydroxyvitamin D3 (1,25-(OH)(2) D(3) ) treatment. Such treatment also decreased the expression of the TNF-α-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)(2) D(3) decreased proinflammatory marker expression under basal and TNF-α-stimulated conditions. The involvement of VDR and NF-κB was confirmed in these regulations. Incubation with 1,25-(OH)(2) D(3) 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)(2) D(3) 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)(2) D(3) 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.
Study Information
Marcotorchino J, Gouranton E, Romier B, Tourniaire F, Astier J, Malezet C, Amiot MJ, Landrier JF.
Vitamin D reduces the inflammatory response and restores glucose uptake in adipocytes.
Mol Nutr Food Res.
2012 December
INRA, UMR1260, Marseille, France; INSERM, UMR1062, «Nutrition, Obesity and Risk of Thrombosis», Marseille, France; Faculté de Médecine, Aix-Marseille University, Marseille, France.
Full Study
