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. Author manuscript; available in PMC: 2017 Mar 21.
Published in final edited form as: Vitam Horm. 2016 Mar 21;101:175–196. doi: 10.1016/bs.vh.2016.02.002

Fig. 1. Role of the miR-34a/βKL/FGF19 axis in liver.

Fig. 1

(A) In diet-induced obese mice, aberrantly elevated hepatic miR-34a represses the expression of the obligate co-receptor for FGF19, βKL, by directly binding to the 3’UTR of the βKL transcript, resulting in attenuation of FGF19 signaling. The impaired FGF19 signaling in obesity leads to increased triglycerides/glucose levels, decreased glycogen levels in the liver, and decreased insulin sensitivity in fatty liver of obese mice. (B) Treatment with anti-miR-34a in dietary obese mice results in downregulation of the elevated miR-34a, increased expression of βKL, and subsequently, improves FGF19 signaling. The improved FGF19 signaling results in increased glycogen levels, decreased triglycerides levels in the liver, and increased insulin sensitivity.