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Journal of Lipid Research, Vol. 49, 1562-1568, July 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology


* Institute of Normal Human Morphology, University of Ancona (Politecnica delle Marche), Ancona, Italy
Department of Urology, University of Ancona (Politecnica delle Marche), Ancona, Italy
This work was supported by grants from the Italian Ministry of University (Cofin 2005 to S.C., FIRB Internazionalizzazione 2005 to S.C., and Università Politecnica delle Marche RSA 2007 to S.C.), and by TOBI EWO6-007 (Targeting Obesity-driven Inflammation).
Published, JLR Papers in Press, April 30, 2008.
1 To whom correspondence should be addressed. e-mail: cinti{at}univpm.it
Accumulation of visceral fat is a key phenomenon in the onset of obesity-associated metabolic disorders. Macrophage infiltration induces chronic mild inflammation widely considered as a causative factor for insulin resistance and eventually diabetes. We previously showed that >90% of macrophages infiltrating the adipose tissue of obese animals and humans are arranged around dead adipocytes, forming characteristic crown-like structures (CLS). In this study we quantified CLS in visceral and subcutaneous depots from two strains of genetically obese mice, db/db and ob/ob. In both strains, CLS were prevalent in visceral compared with subcutaneous fat. Adipocyte size and CLS density exhibited a positive correlation both in visceral and in subcutaneous depots; however, the finding that adipocyte size was smallest and CLS density highest in visceral fat suggests a different susceptibility of visceral and subcutaneous adipocytes to death. Visceral fat CLS density was 3.4-fold greater in db/db than in ob/ob animals, which at the age at which our experimental strain was used are more prone to glucose metabolic disorders.
Supplementary key words obesity macrophages subcutaneous fat adipocyte death
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