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Role of macrophage tissue infiltration in metabolic diseases

Bouloumié, Annea,b; Curat, Cyrile Annea; Sengenès, Coraliea; Lolmède, Karineb; Miranville, Alexandraa; Busse, Rudia

Current Opinion in Clinical Nutrition & Metabolic Care: July 2005 - Volume 8 - Issue 4 - p 347–354
Genes and cell metabolism

Purpose of review: White adipose tissue is necessary for optimal energy homeostasis and the excessive development of fat mass is clearly associated with the metabolic syndrome. The fact that adipocytes secrete a number of specific factors or ‘adipokines’ has forced a reassessment of the involvement of adipose tissue in a wide range of physiological and pathophysiological processes. Obesity has recently been described as a ‘low-grade’ inflammatory condition, a state proposed to represent a common determinator in the genesis of obesity-associated pathologies, i.e. diabetes and atherosclerosis.

Recent findings: Recent reports of an increase in the number of macrophages that infiltrate the fat mass in obese individuals led to the suggestion that adipose tissue itself is a source and site of inflammation.

Summary: This review summarizes recent data on the characterization of the macrophage population in fat tissue. Their origin, fate and activation will be considered. The potential involvement of adipose tissue macrophages in the development of insulin resistance and vascular pathologies, as well as in the control of adipose tissue growth and metabolism, will be examined.

aInstitute of Cardiovascular Physiology, Johann Wolfgang Goethe University, Theodor Stern Kai 7, 60590 Frankfurt am Main, Germany

bObesity Research Unit, INSERM U 586, Louis Bugnard Institute, Centre Hospitalier Universitaire Rangueil, Université Paul Sabatier, Toulouse, France

Correspondence to Anne Bouloumié, Institute of Cardiovascular Physiology, Johann Wolfgang Goethe University, Theodor Stern Kai 7, 60590 Frankfurt am Main, Germany Tel: +49 69 6301 6973; fax: +49 69 6301 7668; e-mail: bouloumie@zphys1.uni-frankfurt.de

© 2005 Lippincott Williams & Wilkins, Inc.