Journal
CELL REPORTS
Volume 14, Issue 10, Pages 2273-2280Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2016.02.026
Keywords
-
Categories
Funding
- NIH [R01 DK107220, R24 DK090963]
- MRC [MC_UP_1102/18] Funding Source: UKRI
- Medical Research Council [MC_UP_1102/18] Funding Source: researchfish
- Pancreatic Cancer UK [RIF2014_07_Tournier] Funding Source: researchfish
Ask authors/readers for more resources
The cJun NH2-terminal kinase (JNK)-signaling pathway is implicated in metabolic syndrome, including dysregulated blood glucose concentration and insulin resistance. Fibroblast growth factor 21 (FGF21) is a target of the hepatic JNK-signaling pathway and may contribute to the regulation of glycemia. To test the role of FGF21, we established mice with selective ablation of the Fgf21 gene in hepatocytes. FGF21 deficiency in the liver caused marked loss of FGF21 protein circulating in the blood. Moreover, the protective effects of hepatic JNK deficiency to suppress metabolic syndrome in high-fat diet-fed mice were not observed in mice with hepatocyte-specific FGF21 deficiency, including reduced blood glucose concentration and reduced intolerance to glucose and insulin. Furthermore, we show that JNK contributes to the regulation of hepatic FGF21 expression during fasting/feeding cycles. These data demonstrate that the hepatokine FGF21 is a key mediator of JNK-regulated metabolic syndrome.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available