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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1211.)
© 2008 American Heart Association, Inc.

Editorials

Adipose Tissue Lymphocytes and Macrophages in Obesity and Insulin Resistance

Makers or Markers, and Which Comes First?

A. Bouloumié; L. Casteilla; M. Lafontan

From the Institut National de la Santé et de la Recherche Médicale (INSERM) (A.B., M.L.), Unité 858 & Université Toulouse III Paul Sabatier, Institut de Médecine Moléculaire de Rangueil, Equipe No. 1 AVENIR, IFR31, BP84225, 31432 Toulouse, France; and UMR 5241 CNRS UPS IFR31 (L.C.), IFR109 Institut Louis Bugnard, BP 84225, 31432 Toulouse Cedex 4, France.

Correspondence to A. Bouloumié, Institut National de la Santé et de la Recherche Médicale (INSERM), Unité 858 & Université Toulouse III Paul Sabatier, Institut de Médecine Moléculaire de Rangueil, Equipe No. 1 AVENIR, IFR31, BP84225, 31432 Toulouse, France. E-mail anne. bouloumie@toulouse.inserm.fr

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Obesity, and more specifically accumulation of adipose tissue in the visceral and subcutaneous abdominal locations, is a major risk factor for the development of cardiovascular pathologies including hypertension and atherosclerosis, as well as metabolic disorders such as type 2 diabetes. During recent years, "metaflammation" or metabolically-triggered inflammation¹ has emerged as a key process involved in the clustering of those conditions. Although several metabolically active organs such as the liver, muscle, and, recently, the intestine² certainly play major roles, the white adipose tissue appears as a central and primary player as both a source and site of inflammation. Accumulation of adipose tissue macrophages (ATMs) has been well-described in obese conditions in mice and humans.^3–5 Moreover, the ATM proinflammatory phenotype has been linked to the development of insulin resistance in mice,⁴ although the exact nature of the proinflammatory myeloid cells, ie, macrophages or dentritic cells, remains to be determined.⁶ Nevertheless, the causal link between inflammation and insulin resistance was further strengthened by the specific knock-out of the inflammation coordinator IkappaB kinase beta of myeloid cells, which gave protection against insulin resistance.⁷ The study of Kintscher and al in this issue⁸ extends those original observations to cells of adaptative immunity. The authors suggest that the accumulation of T-lymphocytes, assessed mainly through gene expression analyses and immunohistochemistry, occurs in the perigonadal adipose tissue of mice on a high-fat diet before the accumulation of macrophages. Moreover, the increased expression of T-lymphocyte markers was concomitant with the initiation of insulin resistance characterized by a reduction in . . . [Full Text of this Article]

Related Article:

T-lymphocyte Infiltration in Visceral Adipose Tissue: A Primary Event in Adipose Tissue Inflammation and the Development of Obesity-Mediated Insulin Resistance

Ulrich Kintscher, Martin Hartge, Katharina Hess, Anna Foryst-Ludwig, Markus Clemenz, Martin Wabitsch, Pamela Fischer-Posovszky, Thomas F.E. Barth, Duska Dragun, Thomas Skurk, Hans Hauner, Matthias Blüher, Thomas Unger, Anna-Maria Wolf, Uwe Knippschild, Vinzenz Hombach, and Nikolaus Marx
Arterioscler Thromb Vasc Biol 2008 28: 1304-1310. [Abstract] [Full Text] [PDF]

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