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Glucose administration inhibits the hepatic activation of gluconeogenesis promoted by insulin-induced hypoglycemia

机译:葡萄糖给药抑制胰岛素诱导的低血糖促进的肝糖异生的肝激活

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The activation of hepatic gluconeogenesis in male Wistar adult 6 h fasted rats during insulin-induced hypoglycemia (IIH) was previously demonstrated. In this study, the effects of intraperitoneal (ip) glucose (100 mg/kg) on the activation of liver gluconeogenesis during IIH was investigated. Thus, 6 h fasted rats that received ip regular insulin (1 U/kg) and 30 min later ip saline (Control group) or glucose (Experimental group) were compared. All the experiments were executed 60 min after insulin injection. The glycemia of Control and Experimental groups were not different (P > 0.05). To investigate gluconeogenesis, liver perfusion experiments were performed. The results demonstrated that excepting glycerol, livers from rats which received ip glucose showed lower (P < 0.05) gluconeogenesis from L-alanine, L-glutamine, L-lactate or L-alanine + L-glutamine + L-lactate + glycerol. Therefore, the absence of glucose recovery after the glucose administration was mediated, at least in part, by an inhibition of hepatic gluconeogenesis.
机译:先前已证明在胰岛素诱导的低血糖症(IIH)期间,在禁食的雄性Wistar成年雄性大鼠6 h中,肝糖异生的激活。在这项研究中,研究了腹膜内(ip)葡萄糖(100 mg / kg)对IIH期间肝糖异生的激活的影响。因此,比较了禁食6 h的腹腔注射普通胰岛素(1 U / kg)和30分钟后的腹腔注射生理盐水(对照组)或葡萄糖(实验组)的大鼠。胰岛素注射后60分钟执行所有实验。对照组和实验组的血糖无差异(P> 0.05)。为了研究糖异生,进行了肝脏灌注实验。结果表明,除甘油外,接受ip葡萄糖的大鼠肝脏显示出较低的(P <0.05)L-丙氨酸,L-谷氨酰胺,L-乳酸或L-丙氨酸+ L-谷氨酰胺+ L-乳酸+甘油的糖异生作用。因此,至少部分地通过抑制肝糖异生来介导葡萄糖给药后葡萄糖恢复的缺乏。

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