Caspary W F, Lücke H
Res Exp Med (Berl). 1976 Feb 27;167(1):1-13. doi: 10.1007/BF02180283.
Endogeneous hyperglucagonemia is observed in experimental diabetes mellitus and semistarvation, conditions associated with an increased intestinal absorptive function. To examine whether glucagon might exert a similar adaptive response on intestinal digestive-absorptive function like experimental diabetes mellitus the effect of chronic glucagon administration on intestinal transport of 3-0-methyl-D-glucose, water, sodium, potassium, and D-glucose induced transmural potential difference (PD) was examined by an in vivo perfusion technique in rat small intestine. Chronic administration of glucagon (100 mug twice daily) for 5 days resulted in increased absorption of 3-0-methyl-D-glucose, water, sodium and potassium as well as in an increase of D-glucose induced PD. A similar, but more pronounced augmentation of D-glucose induced PD was observed in the jejunum of streptozotocin-diabetic rats. Disaccharidase (maltase, sucrase, trehalase, lactase) and alkaline phosphatase activities were not affected in intestinal mucosa of glucagon-treated rats compared to controls. It cannot be decided from these results whether hyperglucagonemia is responsible for the adaptive intestinal changes observed in experimental diabetes mellitus.
在实验性糖尿病和半饥饿状态(与肠道吸收功能增强相关的情况)中观察到内源性高胰高血糖素血症。为了研究胰高血糖素是否可能像实验性糖尿病那样对肠道消化吸收功能产生类似的适应性反应,采用体内灌注技术在大鼠小肠中检测了长期给予胰高血糖素对3 - O - 甲基 - D - 葡萄糖、水、钠、钾以及D - 葡萄糖诱导的跨壁电位差(PD)的肠道转运的影响。每天两次给予胰高血糖素(100微克),持续5天,导致3 - O - 甲基 - D - 葡萄糖、水、钠和钾的吸收增加,以及D - 葡萄糖诱导的PD增加。在链脲佐菌素诱导的糖尿病大鼠的空肠中观察到类似但更明显的D - 葡萄糖诱导的PD增强。与对照组相比,胰高血糖素处理的大鼠肠道黏膜中的双糖酶(麦芽糖酶、蔗糖酶、海藻糖酶、乳糖酶)和碱性磷酸酶活性未受影响。从这些结果无法确定高胰高血糖素血症是否是实验性糖尿病中观察到的肠道适应性变化的原因。