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Adipose tissue remodeling and obesity
Kai Sun, … , Christine M. Kusminski, Philipp E. Scherer
Kai Sun, … , Christine M. Kusminski, Philipp E. Scherer
Published June 1, 2011
Citation Information: J Clin Invest. 2011;121(6):2094-2101. https://doi.org/10.1172/JCI45887.
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Review Series

Adipose tissue remodeling and obesity

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Abstract

To fulfill its role as the major energy-storing tissue, adipose has several unique properties that cannot be seen in any other organ, including an almost unlimited capacity to expand in a non-transformed state. As such, the tissue requires potent mechanisms to remodel, acutely and chronically. Adipocytes can rapidly reach the diffusional limit of oxygen during growth; hypoxia is therefore an early determinant that limits healthy expansion. Proper expansion requires a highly coordinated response among many different cell types, including endothelial precursor cells, immune cells, and preadipocytes. There are therefore remarkable similarities between adipose expansion and growth of solid tumors, a phenomenon that presents both an opportunity and a challenge, since pharmacological interventions supporting healthy adipose tissue adaptation can also facilitate tumor growth.

Authors

Kai Sun, Christine M. Kusminski, Philipp E. Scherer

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Figure 1

Healthy and unhealthy AT expansion.

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Healthy and unhealthy AT expansion.
(A) Healthy AT expansion consists of...
(A) Healthy AT expansion consists of an enlargement of AT through effective recruitment of adipogenic precursor cells to the adipogenic program, along with an adequate angiogenic response and appropriate remodeling of the ECM. There are strong individual differences with respect to the potential for AT expansion. (B) In contrast, pathological AT expansion consists of massive enlargement of existing adipocytes, limited angiogenesis, and ensuing hypoxia. As a result, HIF-1α is induced, which in turn can cause the induction of a fibrotic program. Ultimately, M1-stage macrophages prevail, leading to an inflammatory phenotype that is strongly associated with systemic insulin resistance.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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