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13 septembre 2011 2 13 /09 /septembre /2011 18:01

 

 

L'obésité est liée à l'inflammation des tissus adipeux blancs, accompagnée d'une infiltration par les macrophages. 

Il vient d'être démontré que la QUERCITINE - extraite de la poudre de raisin - réduit cette inflammation au niveau des macrophages hummains, et l'insulino résistance au niveau es adipocytes humains. 

 

 

 

 

International Journal of Obesity 35, 1165-1172 (September 2011) | doi:10.1038/ijo.2010.272

 

Quercetin attenuates inflammation in human macrophages and adipocytes exposed to macrophage-conditioned media

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A Overman, C-C Chuang and M McIntosh

Abstract

Background:

Obesity is linked to chronic inflammation in white adipose tissue, which is exacerbated by infiltrating macrophages (MΦs). We recently demonstrated that an extract from grape powder (GPE), which is abundant in quercetin (QUE), reduced inflammation in human MΦs and prevented MΦ-mediated inflammation and insulin resistance in human adipocytes. However, we did not know how QUE individually affected these outcomes.

 

Objective and design:

We examined the extent to which QUE prevents inflammation in human MΦs (that is, differentiated U937 cell line) and cross-talk with human adipocytes (that is, primary cultures of newly differentiated human adipocytes).

 

Methods and results:

Treatment of MΦs with QUE attenuated the basal expression of inflammatory genes, such as tumor necrosis factor-α, interleukin (IL)-6, IL-8, IL-1β and interferon-γ inducible protein-10, and cyclooxygenase-2, a marker of prostaglandin production. QUE also attenuated the abundance of phosphorylated c-Jun N-terminal kinase (JNK) and c-Jun, and IκBα degradation in MΦs. Furthermore, conditioned media (CM) obtained from MΦs treated with QUE decreased the capacity of this CM to inflame adipocytes and cause insulin resistance as evidenced by decreased: (1) inflammatory gene expression, (2) phosphorylation of JNK and c-Jun, (3) serine residue 307 phosphorylation of insulin receptor substrate (IRS)-1, 4) protein tyrosine phosphatase-1B gene expression and 5) suppression of insulin-stimulated glucose uptake.

 

Conclusion:

Taken together, these data suggest that QUE is one of the bioactive components of GPE that prevents inflammation in MΦs and MΦ-mediated insulin resistance in adipocytes.

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