Research ArticleMetabolic Disease

Development of a therapeutic monoclonal antibody that targets secreted fatty acid–binding protein aP2 to treat type 2 diabetes

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Science Translational Medicine  23 Dec 2015:
Vol. 7, Issue 319, pp. 319ra205
DOI: 10.1126/scitranslmed.aac6336

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Kill the messenger

A variety of metabolic messengers—many from adipose tissue itself—controls the energy state of organs and organisms. Recently, researchers showed that the fatty acid binding protein aP2, once thought to live and work only in the cytoplasm, is also secreted by adipose tissue and spurs metabolic changes in other organs. Now, Burak and colleagues test whether secreted aP2 can serve as a therapeutic target for type 2 diabetes.

In mice, the secreted form of aP2 regulates glucose production in liver, systemic glucose homeostasis, and insulin resistance. Serum levels of aP2 were shown to be elevated in obese mice and humans and to correlate with metabolic complications. The authors identified a monoclonal antibody to aP2 that lowered fasting blood glucose, increased insulin sensitivity, and lowered both fat mass and fatty liver (steatosis) in obese mouse models, relative to a control antibody, but not in aP2-deficient mice. The antidiabetic effects of the therapeutic antibody were linked to the regulation of hepatic glucose output and peripheral glucose utilization. Together, these findings suggest that an aP2-targeted antibody that kills the messenger is a viable approach for diabetes treatment.

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