Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Dec 22:2013:139239.
doi: 10.1155/2013/139239.

Adipose tissue in obesity-related inflammation and insulin resistance: cells, cytokines, and chemokines

Affiliations
Review

Adipose tissue in obesity-related inflammation and insulin resistance: cells, cytokines, and chemokines

Kassem Makki et al. ISRN Inflamm. .

Abstract

Adipose tissue is a complex organ that comprises a wide range of cell types with diverse energy storage, metabolic regulation, and neuroendocrine and immune functions. Because it contains various immune cells, either adaptive (B and T lymphocytes; such as regulatory T cells) or innate (mostly macrophages and, more recently identified, myeloid-derived suppressor cells), the adipose tissue is now considered as a bona fide immune organ, at the cross-road between metabolism and immunity. Adipose tissue disorders, such as those encountered in obesity and lipodystrophy, cause alterations to adipose tissue distribution and function with broad effects on cytokine, chemokine, and hormone expression, on lipid storage, and on the composition of adipose-resident immune cell populations. The resulting changes appear to induce profound consequences for basal systemic inflammation and insulin sensitivity. The purpose of this review is to synthesize the current literature on adipose cell composition remodeling in obesity, which shows how adipose-resident immune cells regulate inflammation and insulin resistance-notably through cytokine and chemokine secretion-and highlights major research questions in the field.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Adipose tissue-resident cells, cytokines, and hormones: role in insulin sensitivity (adapted and updated from [7]).

Similar articles

Cited by

References

    1. Hotamisligil GS, Erbay E. Nutrient sensing and inflammation in metabolic diseases. Nature Reviews Immunology. 2008;8(12):923–934. - PMC - PubMed
    1. Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annual Review of Immunology. 2011;29:415–445. - PubMed
    1. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860–867. - PubMed
    1. Ouchi N, Parker JL, Lugus JJ, Walsh K. Adipokines in inflammation and metabolic disease. Nature Reviews Immunology. 2011;11(2):85–97. - PMC - PubMed
    1. Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. The Journal of Clinical Investigation. 2006;116(7):1793–1801. - PMC - PubMed