LAUSR

Over a decade ago, fibroblast growth factor 21 (FGF21) was identified as a novel regulator of metabolism (1). Since that time, accumulating data have substantiated the therapeutic potential of this hormone in counteracting metabolic disease. Increasing levels of FGF21 in mice, either through transgenic overexpression or exogenous administration, has consistently produced favorable effects on obesity and its sequelae. Mechanistically, FGF21 has been shown to promote browning of adipose tissue, increase thermogenesis, and enhance energy expenditure. Although the limited experience using exogenous FGF21 in human trials is encouraging (2), boosting endogenous FGF21 production by manipulating its physiologic regulatory mechanisms is viewed as an exciting alternative, yet unproven, therapeutic strategy. This article is protected by copyright. All rights reserved.