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Biochem Biophys Res Commun. 2008 Dec 19;377(3):987-91. doi: 10.1016/j.bbrc.2008.10.088. Epub 2008 Oct 24.

Role of GPR81 in lactate-mediated reduction of adipose lipolysis.

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Department of Cardiovascular Diseases, Merck Research Laboratories, RY80T-A100, 126 East Lincoln Avenue, Rahway, NJ 07065, USA.


Heavy exercise or oxygen deficit often links with higher levels of arterial lactate and lower levels of plasma free fatty acids (FFA). Treatment with lactate reduces circulating levels of FFA in vivo and lipolysis in adipose tissues in vitro. However, the underlying mechanism has remained unclear. Here we employ pharmacological and genetic approaches to show that GPR81, an orphan G-protein-coupled receptor with relatively restricted expression in the adipose tissues, functions as a receptor for lactate and can mediate an anti-lipolytic effect of lactate. GPR81 may thus function as a sensor of lactate that can modulate the FFA pool under exercise or conditions of oxygen deficit.

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