1. Recent studies suggest that a local hypoxic response leads to chronic inflammation in the adipose tissue of obese individuals. The adipose tissue hypoxia may reflect a compensatory failure in the local vasculature system in response to obesity. 2. Studies suggest that inflammation stimulates angiogenesis and inhibits adipocyte activities in a feedback manner within the obese adipose tissue. Adipose-derived stem cells (ASC) are able to differentiate into multiple lineages of progenitor cells for adipocytes, endothelial cells, fibroblasts and pericytes. Differentiation of ASC into those progenitors is regulated by the adipose tissue microenvironment. 3. As a major factor in the microenvironment, inflammation may favour ASC differentiation into endothelial cells through the induction of angiogenic factors. At the same time, inflammation inhibits ASC differentiation into adipocytes by suppressing peroxisome proliferator-activated receptor γ activity and the insulin signalling pathway. In this context, inflammation may serve as a signal mediating the competition between adipocytes and endothelial cells for the limited source of ASC. 4. It is a new concept that inflammation mediates signals in the competition between adipocytes and endothelial cells for the limited ASC in obesity. There is a lot of evidence that inflammation promotes endothelial cell differentiation. However, this activity of inflammation remains to be established in adipose tissue. The present article reviews the literature in support of this conclusion.
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| http://dx.doi.org/10.1111/j.1440-1681.2011.05596.x | DOI Listing |
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