Serum fibroblast growth factor 19 (FGF19) levels are associated with atherogenic dyslipidemia in patients with type 2 diabetes

Hu, Jingyi; Zou, Hailan; Li, Yanhua; Nie, Dong-Ying; Chen, Chao; Liu, Jin-Han; Ding, Jin; Zhang, Zhou; Xiao, Yang

doi:10.1097/cm9.0000000000001574

Cited by 1 publication

(1 citation statement)

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“…To stabilize SHP and dampen Cyp7a1 production, FGF19 functions as an endocrine hormone by attaching to the fibroblast growth factor receptor 4 (FGFR4)/ β-Klotho complex, which prevents the synthesis of BA [7][8][9][10]. Recently, FGF19 has been identified as a promising therapeutic target for diabetes, cholestatic liver disease, nonalcoholic steatohepatitis (NASH), and abnormalities of BA metabolism as a result of its remarkable pharmacological capabilities [11][12][13][14]. However, there are significant safety concerns due to the fact that long-term treatment with wild type FGF19 (FGF19 WT ) increases hepatocellular carcinoma [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Engineered FGF19ΔKLB protects against intrahepatic cholestatic liver injury in ANIT-induced and Mdr2-/- mice model

Shi,

Zhao,

Huang

et al. 2023

BMC Biotechnol

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Background The major safety concern of the clinical application of wild type FGF19 (FGF19WT) emerges given that its extended treatment causes hepatocellular carcinoma. Therefore, we previously generated a safer FGF19 variant - FGF19ΔKLB, which have same effects on glycemic control and bile acid production but much less mitogenic activity. However, it remains unclear as to whether FGF19ΔKLB ameliorates intrahepatic cholestasis. Results We found that, similar to that of FGF19WT, the chronic administration of FGF19ΔKLB protects mice from cholestatic liver injury in these two models. The therapeutic benefits of FGF19ΔKLB on cholestatic liver damage are attributable, according to the following mechanistic investigation, to the reduction of BA production, liver inflammation, and fibrosis. More importantly, FGF19ΔKLB did not induce any tumorigenesis effects during its prolonged treatment. Conclusions Together, our findings raise hope that FGF19ΔKLB may represent a useful therapeutic strategy for the treatment of intrahepatic cholestasis.

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