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Obesity and metabolic disease: is adipose tissue the culprit?

Abstract:
Obesity is a risk factor for the development of type 2 diabetes and CVD. Is adipose tissue the culprit in the relationship between obesity and metabolic disease? It is certainly possible to argue that adipose tissue function is disturbed in obesity in such a way that adverse consequences may follow. For instance, lipolysis is down regulated, the sensitivity of lipolysis to insulin is reduced and there are disturbances in the regulation of adipose tissue blood flow. However, when examined critically these changes can be seen as adaptations to the increased adipose tissue mass, making the situation better rather than worse. In terms of the many peptide and other factors now known to be secreted from adipose tissue, it is easier to argue that adipose tissue is the culprit. However, for no single 'adipokine' is there as yet unequivocal evidence of a link between adipose tissue secretion and adverse metabolic events in other tissues. The best documented of these adipokines in relation to insulin resistance is adiponectin. Here, unusually, adiponectin confers insulin sensitivity, and its secretion is down regulated in obesity. It could be again that adipose tissue has down regulated its function in an attempt to compensate for its increased mass, although certainly that down-regulation is too extreme. On balance, it is clear that adipose tissue is a link in the chain of events leading to metabolic disease, but in many respects it is an innocent intermediary trying to deal with the consequences of positive energy balance, the real culprit.
Publication status:
Published

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Publisher copy:
10.1079/pns2004403

Authors


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Institution:
University of Oxford
Division:
MSD
Department:
RDM
Sub department:
OCDEM
Role:
Author


Journal:
Proceedings of the Nutrition Society More from this journal
Volume:
64
Issue:
1
Pages:
7-13
Publication date:
2005-02-01
Event title:
Summer Meeting of the Nutrition-Society/Association-for-the-Study-of-Ovesity
DOI:
EISSN:
1475-2719
ISSN:
0029-6651


Keywords:
Pubs id:
pubs:29524
UUID:
uuid:73e2bf4e-e5ea-4061-a9f7-6b5b459e8bfe
Local pid:
pubs:29524
Source identifiers:
29524
Deposit date:
2012-12-19

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