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高血糖会诱导胰腺次全切除大鼠的肠道蔗糖酶活性。

Hyperglycemia induces intestinal sucrase activity in subtotally pancreatectomized rats.

作者信息

Takeguchi T, Mori K, Takano S, Akagi M

出版信息

Gastroenterol Jpn. 1985 Feb;20(1):20-7. doi: 10.1007/BF02774670.

Abstract

The effects of experimental diabetes, hypertonic glucose infusion, and subsequent insulin administration on the sucrase activity of the small intestine were studied using intestinal segments completely excluded from luminal continuity by construction of Thiry-Vella fistulas in rats. Eight weeks after subtotal pancreatectomy, the rats contracted insulin-deficient diabetes mellitus, and sucrase activity was enhanced in both the Thiry-Vella loop and in the proximal jejunum in continuity. Subcutaneous injections of insulin during the last 4 weeks maintained the enzyme activity in the control range in both segments. There was a positive correlation between sucrase activity and blood glucose level in the pancreatectomized rats. Hyperglycemia in normal rats induced by intravenous infusion of 30% glucose solution over 48 hours enhanced the sucrase activity in the jejunum. Furthermore, insulin administration with a glucose solution inhibited the enhancement of enzyme activity. These findings suggest that hyperglycemia itself might play an important role in the diabetic increment of sucrase activity.

摘要

通过在大鼠身上构建Thiry-Vella瘘管,将肠段与肠腔完全隔离,研究了实验性糖尿病、高渗葡萄糖输注以及随后给予胰岛素对小肠蔗糖酶活性的影响。在进行胰腺次全切除术后8周,大鼠患上胰岛素缺乏型糖尿病,Thiry-Vella肠袢和与之相连的空肠近端的蔗糖酶活性均增强。在最后4周皮下注射胰岛素可使两个肠段的酶活性维持在对照范围内。在胰腺切除的大鼠中,蔗糖酶活性与血糖水平呈正相关。通过静脉输注30%葡萄糖溶液48小时诱导正常大鼠出现高血糖,可增强空肠中的蔗糖酶活性。此外,用葡萄糖溶液同时给予胰岛素可抑制酶活性的增强。这些发现表明,高血糖本身可能在糖尿病时蔗糖酶活性增加中起重要作用。

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