首页> 美国卫生研究院文献>Biochemical Journal >Suppressive effect of insulin on the synthesis of sucrase-isomaltase complex in small intestinal epithelial cells and abnormal increase in the complex under diabetic conditions.
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Suppressive effect of insulin on the synthesis of sucrase-isomaltase complex in small intestinal epithelial cells and abnormal increase in the complex under diabetic conditions.

机译:胰岛素对小肠上皮细胞中蔗糖酶-异麦芽糖酶复合物的合成具有抑制作用并且在糖尿病条件下复合物异常增加。

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摘要

An abnormally high level of the sucrase-isomaltase (SI) complex in the small intestine of rats with streptozotocin-induced insulin-dependent diabetes mellitus (IDDM) was normalized in 11 h by the administration of insulin, in addition to normalization of the blood glucose level. Phlorizin, an inhibitor of renal glucose reabsorption, also caused normalization of the blood glucose level in the IDDM rats; however, the level of the SI complex was barely changed. When mucosa explants were cultured in a medium, the SI complex synthesized during the cultivation was accumulated as its precursor protein without maturation, owing to the absence of pancreatic proteases, and the amount of the precursor protein that accumulated in the explants was decreased by the addition of insulin into the medium. Further, the mRNA level of the SI complex in the explants incubated with insulin was obviously lower than that in the absence of insulin. These results indicate that insulin has a suppressive effect on the synthesis of the SI complex, presumably by decreasing the transcriptional level of the gene encoding the complex, in small-intestinal epithelial cells. Thus the synthesis of the SI complex might exceed normal levels in the epithelial cells as a direct result of the depletion of insulin under IDDM conditions.
机译:除血糖正常化外,还可以在11小时内通过胰岛素注射使链脲佐菌素诱导的胰岛素依赖型糖尿病(IDDM)大鼠小肠中的蔗糖酶-异麦芽糖酶(SI)复合物异常高水平正常化水平。 Phlorizin,一种肾脏葡萄糖重吸收抑制剂,也引起IDDM大鼠血糖水平正常化。但是,SI复合体的级别几乎没有变化。当在培养基中培养粘膜外植体时,由于胰腺蛋白酶的缺乏,在培养过程中合成的SI复合物作为其前体蛋白积累而没有成熟,并且通过添加减少了在外植体中积累的前体蛋白的量。胰岛素注入培养基。此外,与胰岛素一起孵育的外植体中SI复合物的mRNA水平明显低于没有胰岛素的情况。这些结果表明,在小肠上皮细胞中,胰岛素可能通过降低编码该复合物的基因的转录水平而对SI复合物的合成具有抑制作用。因此,在IDDM条件下,胰岛素消耗的直接结果是SI复合物的合成可能超过上皮细胞的正常水平。

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