It is now well recognized that both adipocytes and macrophages that infiltrate adipose tissue help increase systemic inflammation and insulin resistance, which lead to the development of the metabolic syndrome, an important risk factor for type 2 diabetes and cardiovascular disease. In order to examine the contribution of fatty acid-binding proteins (FABPs) to local and systemic inflammation and insulin resistance in mice, Furuhashi et al. used deletion of FABPs separately in adipose tissue and macrophages to study the effect of these deletions of one cell type on the other cell type. Deletion of FABPs in adipocytes was found to reduce cytokine release in macrophages, whereas deletion of FABPs in macrophages enhanced insulin signalling and glucose uptake in adipose tissue. To further investigate the role of FABPs in insulin action and cytokine release, mice with FABP deficiency in bone marrow were engineered. It was found that FABP deficiency in bone marrow-derived elements provided significant protection against the development of insulin resistance in wild-type recipient mice with intact adipocytes. Altogether, these results strengthen the idea that interaction between adipocytes and macrophages within adipose tissue is crucial for the inflammatory basis of the metabolic syndrome and that FABPs may play a critical role in this process. These observations also led the authors to suggest that aP2 inhibitors might warrant further consideration in order to protect adipose tissue from the consequences of macrophage infiltration.
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