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Vitamin D reduces the inflammatory response and restores glucose uptake in adipocytes
Author(s) -
Marcotorchino Julie,
Gouranton Erwan,
Romier Beatrice,
Tourniaire Franck,
Astier Julien,
Malezet Christiane,
Amiot MarieJosèphe,
Landrier JeanFrançois
Publication year - 2012
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201200383
Subject(s) - proinflammatory cytokine , medicine , endocrinology , inflammation , vitamin d and neurology , adipose tissue , adipocyte , vitamin d deficiency , context (archaeology) , chemistry , biology , paleontology
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 (m RNA and protein level) in human adipocytes and in 3 T 3‐ L 1 adipocytes were observed after 1,25‐dihydroxyvitamin D 3 (1,25‐( OH ) 2 D 3 ) treatment. Such treatment also decreased the expression of the TNF ‐α‐mediated proinflammatory marker in 3 T 3‐ L 1 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 ‐κ B 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 D usp 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.