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Inflammation and impaired adipogenesis in hypertrophic obesity in man

Journal article
Authors Birgit Gustafson
Silvia Gogg
Shahram Hedjazifar
Lachmi E Jenndahl
Ann Hammarstedt
Ulf Smith
Published in Am J Physiol Endocrinol Metab
Volume 297
Pages E999-E1003
ISSN 0193-1849 (Print)
Publication year 2009
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Pages E999-E1003
Language en
Subject categories Medical and Health Sciences


Obesity is mainly associated with adipose cell enlargement in adult man (hypertrophic obesity) while the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of BMI, is negatively correlated with whole-body insulin sensitivity. We here review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue including local cellular insulin resistance with reduced IRS-1 and GLUT-4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accumulation; a well-known finding in these individuals and which promotes insulin resistance and cardiometabolic risk. We also review recent results showing that TNFalpha, but not MCP-1, resistin or IL-6, completely prevents normal adipogenesis in preadipocytes, activates Wnt signaling and induces a macrophage-like phenotype in the preadipocytes. In fact, activated preadipocytes, rather than macrophages, may completely account for the increased release of chemokines and cytokines by the adipose tissue in obesity. Understanding the molecular mechanisms for the impaired preadipocyte differentiation in the subcutaneous adipose tissue in hypertrophic obesity is a priority since it may lead to new ways of treating obesity and its associated metabolic complications. Key words: Wnt signaling, TNFalpha, adipose cells, obesity.

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