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Curr Diab Rep. 2015 Nov;15(11):92. doi: 10.1007/s11892-015-0670-x.

Adipose tissue inflammation in the pathogenesis of type 2 diabetes.

Author information

1
Division of Rheumatology, Immunology and Allergy, Department of Medicine Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ayano_Kohlgruber@dfci.harvard.edu.
2
Division of Rheumatology, Immunology and Allergy, Department of Medicine Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. llynch@bwh.harvard.edu.
3
Division of Endocrinology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. llynch@bwh.harvard.edu.

Abstract

At least 2.8 million people die each year as a result of being overweight or obese, and the biggest burden being obesity-related diseases. Overweight and obesity account for a major proportion of type 2 diabetes (T2D) cases. Obesity is associated with inflammation in adipose tissue, namely an infiltration and expansion of macrophages, which produce inflammatory cytokines that interfere with insulin signaling, and a loss of protective cells that promote adipose homeostasis. Thus, it is now clear that inflammation is an underlying cause or contributor to T2D as well as many other obesity-induced diseases, including atherosclerosis and cancer. Inflammatory pathways contribute to impaired glucose handling by adipocytes, hepatocytes, and muscle cells and interfere with insulin production and insulin signaling. This review highlights the roles of the different immune populations in lean adipose tissue and their importance in tissue homeostasis to keep inflammation at bay. We also discuss the changes that occur in these immune cells during the development of obesity, which has detrimental effects on the health of adipose tissue, and local and systemic insulin resistance.

KEYWORDS:

Adipose tissue; Immune system; Inflammation; Innate immunity; Obesity; Type 2 diabetes

PMID:
26374569
DOI:
10.1007/s11892-015-0670-x
[Indexed for MEDLINE]

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