| First Author | Wu G | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 497 |
| Issue | 1 | Pages | 46-50 |
| PubMed ID | 29448103 | Mgi Jnum | J:271992 |
| Mgi Id | MGI:6276820 | Doi | 10.1016/j.bbrc.2018.01.189 |
| Citation | Wu G, et al. (2018) FGF 21 deficiency slows gastric emptying and reduces initial blood alcohol concentration in mice exposed to acute alcohol in fasting state. Biochem Biophys Res Commun 497(1):46-50 |
| abstractText | Excess alcohol consumption can lead to alcoholic liver disease. Fibroblast growth factor 21 (FGF21) is a metabolic regulator with multiple physiologic functions. Previous study demonstrated that FGF21 deficiency exacerbated alcohol-induced liver injury and exogenous FGF21 administration protected liver from chronic alcohol-induced injury. In this study, we aimed to explore the role of FGF21 in alcohol metabolism in mice. FGF21 knockout (KO) mice and the wild type(WT) control mice were divided into two groups and fasted for 24h followed by a bonus of alcohol treatment at a dose of 5g/kg body weight via gavage. Serum alcohol concentration was measured after gavage at 0.5, 2, 3, 4 and 6h, respectively. At the end, gastric and liver tissues were collected. Serum alcohol concentration of KO mice was significantly lower than that of WT at 0.5h after alcohol expose. There were no significant differences in alcohol dehydrogenase (ADH) activity and aldehyde dehydrogenase 2 (ALDH2) activity in gastric and liver tissues between WT and the KO mice. However, gastric emptying time of KO mice was much longer than that of WT mice. In addition, the intestinal permeability and serum GLP-1 level of KO mice were significantly higher than that of WT mice. These results suggest that FGF21 deficiency slow gastric emptying rate and indirectly influence initial alcohol metabolism in mice exposed to acute alcohol. Our findings provide additional information for understanding the gastrointestinal mechanism of alcoholic liver disease and other alcohol use disorders. |
