Kucera T, Jungermann K, Stümpel F
Institute of Biochemistry and Molecular Cell Biology, Georg-August-University, Humboldtallee 23, 37073, Göttingen, Germany.
FEBS Lett. 2000 Jun 2;474(2-3):223-7. doi: 10.1016/s0014-5793(00)01608-2.
In the isolated, jointly perfused small intestine and liver of rats insulin, infused into the portal vein, induced an increase in intestinal glucose absorption via hepatoenteral cholinergic nerves. The possible loss of function of these nerves due to ethanol-induced neuropathy was investigated with 6 weeks ethanol-fed rats. Portal insulin or arterial carbachol failed to increase intestinal glucose absorption but cAMP still did so. The intact stimulatory effect of cAMP indicated an undisturbed capacity of the enterocytes. The loss of action of portal insulin and of arterial carbachol can be explained by the impairment of the hepatoenteral nerves in line with an ethanol-induced neuropathy.
在大鼠离体的、联合灌注的小肠和肝脏中,经门静脉注入胰岛素可通过肝肠胆碱能神经促进肠道葡萄糖吸收。本研究使用经6周乙醇喂养的大鼠,探究了乙醇诱导的神经病变导致这些神经功能可能丧失的情况。门静脉注射胰岛素或动脉注射卡巴胆碱均无法增加肠道葡萄糖吸收,但环磷酸腺苷(cAMP)仍可增加其吸收。cAMP完整的刺激作用表明肠上皮细胞功能未受影响。门静脉胰岛素和动脉卡巴胆碱作用的丧失可通过肝肠神经功能受损来解释,这与乙醇诱导的神经病变相符。