Immune modulation of brown(ing) adipose tissue in obesity
Obesity is associated with a variety of medical conditions such as type 2 diabetes and cardiovascular diseases and is therefore responsible for high morbidity and mortality rates. Increasing energy expenditure by brown adipose tissue (BAT) is a current novel strategy to reduce the excessive energy s...
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Published in | Endocrine reviews Vol. 38; no. 1; pp. 46 - 68 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Washington, DC
Endocrine Society
01.02.2017
Copyright Oxford University Press Oxford University Press |
Subjects | |
Online Access | Get full text |
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Summary: | Obesity is associated with a variety of medical conditions such as type 2 diabetes and cardiovascular diseases and is therefore responsible for high morbidity and mortality rates. Increasing energy expenditure by brown adipose tissue (BAT) is a current novel strategy to reduce the excessive energy stores in obesity. Brown adipocytes burn energy to generate heat and are mainly activated upon cold exposure. As prolonged cold exposure is not a realistic therapy, researchers worldwide are searching for novel ways to activate BAT and/or induce beiging of WAT. Recently the contribution of immune cells in the regulation of brown adipocyte activity and beiging of WAT has gained increased attention, with a prominent role for eosinophils and alternatively activated macrophages. This review will discuss the re-discovery of BAT, present an overview of modes of activation and differentiation of beige and brown adipocytes and describe the recently discovered immunological pathways that are key in mediating brown/beige adipocyte development and function. Interventions in immunological pathways harbour the potential to provide novel strategies to increase beige and brown adipose tissue activity as therapeutic target for obesity. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0163-769X 1945-7189 |
DOI: | 10.1210/er.2016-1066 |