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JOURNAL ARTICLE

FGF15/19 regulates hepatic glucose metabolism by inhibiting the CREB-PGC-1α pathway

Matthew J Potthoff, Jamie Boney-Montoya, Mihwa Choi, Tianteng He, Nishanth E Sunny, Santhosh Satapati, Kelly Suino-Powell, H Eric Xu, Robert D Gerard, Brian N Finck, Shawn C Burgess, David J Mangelsdorf, Steven A Kliewer
Cell Metabolism 2011 June 8, 13 (6): 729-38
21641554
Regulation of hepatic carbohydrate homeostasis is crucial for maintaining energy balance in the face of fluctuating nutrient availability. Here, we show that the hormone fibroblast growth factor 15/19 (FGF15/19), which is released postprandially from the small intestine, inhibits hepatic gluconeogenesis, like insulin. However, unlike insulin, which peaks in serum 15 min after feeding, FGF15/19 expression peaks approximately 45 min later, when bile acid concentrations increase in the small intestine. FGF15/19 blocks the expression of genes involved in gluconeogenesis through a mechanism involving the dephosphorylation and inactivation of the transcription factor cAMP regulatory element-binding protein (CREB). This in turn blunts expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and other genes involved in hepatic metabolism. Overexpression of PGC-1α blocks the inhibitory effect of FGF15/19 on gluconeogenic gene expression. These results demonstrate that FGF15/19 works subsequent to insulin as a postprandial regulator of hepatic carbohydrate homeostasis.

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