Format

Send to

Choose Destination
Clin Sci (Lond). 2016 Sep 1;130(18):1603-14. doi: 10.1042/CS20160005.

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

Author information

1
Department of Medicine, University of Leipzig, Leipzig 04103, Germany bluma@medizin.uni-leipzig.de.

Abstract

The worldwide obesity epidemic has become a major health concern, because it contributes to higher mortality due to an increased risk for noncommunicable diseases including cardiovascular diseases, type 2 diabetes, musculoskeletal disorders and some cancers. Insulin resistance may link accumulation of adipose tissue in obesity to metabolic diseases, although the underlying mechanisms are not completely understood. In the past decades, data from human studies and transgenic animal models strongly suggested correlative, but also causative associations between activation of proinflammatory pathways and insulin resistance. Particularly chronic inflammation in adipose tissue seems to play an important role in the development of obesity-related insulin resistance. On the other hand, adipose tissue inflammation has been shown to be essential for healthy adipose tissue expansion and remodelling. However, whether adipose tissue inflammation represents a consequence or a cause of impaired insulin sensitivity remains an open question. A better understanding of the molecular pathways linking excess adipose tissue storage to chronic inflammation and insulin resistance may provide the basis for the future development of anti-inflammatory treatment strategies to improve adverse metabolic consequences of obesity. In this review, potential mechanisms of adipose tissue inflammation and how adipose tissue inflammation may cause insulin resistance are discussed.

KEYWORDS:

adipocytes; adipokines; adipose tissue inflammation; adipose tissue macrophages; insulin resistance; obesity

PMID:
27503945
DOI:
10.1042/CS20160005
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center