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DOI 10.3389/fphar.2020.00052

Медицинская библиотека · Frontiers in pharmacology · 2020

Fibroblast Growth Factor 1 Ameliorates Diabetes-Induced Liver Injury by Reducing Cellular Stress and Restoring Autophagy.

Xu Zeping, Wu Yanqing, Wang Fan, Li Xiaofeng, Wang Ping, Li Yuying, Wu Junnan, Li Yiyang, Jiang Ting, Pan Xindian, Zhang Xie, Xie Longteng, Xiao Jian, Liu Yanlong

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Аннотация

BACKGROUND

Type 2 diabetes (T2D) is a metabolic dysfunction disease that causes several complications. Liver injury is one of these that severely affects patients with diabetes. Fibroblast growth factor 1 (FGF1) has glucose-lowering activity and plays a role in modulation of several liver injuries. Nevertheless, the effects and potential mechanisms of FGF1 against diabetes-induced liver injury are unknown.

METHODS

To further investigate the effect of FGF1 on diabetic liver injury, we divided db/db mice into two groups and intraperitoneally (i.p.) injected either with FGF1 at 0.5 mg/kg body weight or saline every other day for 4 weeks. Then body weights were measured. Serum and liver tissues were collected for biochemical and molecular analyses.

RESULTS

FGF1 significantly reduced blood glucose and ameliorated diabetes-induced liver steatosis, fibrosis, and apoptosis. FGF1 also restored defective hepatic autophagy in db/db mice. Mechanistic investigations showed that diabetes markedly induced oxidative stress and endoplasmic reticulum stress and that FGF1 treatment significantly attenuated these effects.

CONCLUSIONS

FGF1-associated glucose level reduction and amelioration of cellular stress are potential protective effects of FGF1 against diabetes-induced liver injury.

Для цитирования: Xu Zeping, Wu Yanqing, Wang Fan, Li Xiaofeng, Wang Ping, Li Yuying, Wu Junnan, Li Yiyang, Jiang Ting, Pan Xindian, Zhang Xie, Xie Longteng, Xiao Jian, Liu Yanlong. Fibroblast Growth Factor 1 Ameliorates Diabetes-Induced Liver Injury by Reducing Cellular Stress and Restoring Autophagy.. Frontiers in pharmacology. 2020. DOI: 10.3389/fphar.2020.00052.
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