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Published in: Diabetology & Metabolic Syndrome 1/2012

Open Access 01-12-2012 | Review

Targeting adipose tissue

Authors: Bodo Haas, Paul Schlinkert, Peter Mayer, Niels Eckstein

Published in: Diabetology & Metabolic Syndrome | Issue 1/2012

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Abstract

Two different types of adipose tissues can be found in humans enabling them to respond to starvation and cold: white adipose tissue (WAT) is generally known and stores excess energy in the form of triacylglycerol (TG), insulates against cold, and serves as a mechanical cushion. Brown adipose tissue (BAT) helps newborns to cope with cold. BAT has the capacity to uncouple the mitochondrial respiratory chain, thereby generating heat rather than adenosine triphosphate (ATP). The previously widely held view was that BAT disappears rapidly after birth and is no longer present in adult humans. Using positron emission tomography (PET), however, it was recently shown that metabolically active BAT occurs in defined regions and scattered in WAT of the adult and possibly has an influence on whole-body energy homeostasis. In obese individuals adipose tissue is at the center of metabolic syndrome. Targeting of WAT by thiazolidinediones (TZDs), activators of peroxisome proliferator-activated receptor γ (PPARγ) a ‘master’ regulator of fat cell biology, is a current therapy for the treatment of type 2 diabetes. Since its unique capacity to increase energy consumption of the body and to dissipate surplus energy as heat, BAT offers new perspectives as a therapeutic target for the treatment of obesity and associated diseases such as type 2 diabetes and metabolic syndrome. Recent discoveries of new signaling pathways of BAT development give rise to new therapeutic possibilities in order to influence BAT content and activity.
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Metadata
Title
Targeting adipose tissue
Authors
Bodo Haas
Paul Schlinkert
Peter Mayer
Niels Eckstein
Publication date
01-12-2012
Publisher
BioMed Central
Published in
Diabetology & Metabolic Syndrome / Issue 1/2012
Electronic ISSN: 1758-5996
DOI
https://doi.org/10.1186/1758-5996-4-43

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