Study on the regulation of sucrase-isomaltase mRNA in the small intestine

小肠蔗糖酶异麦芽酶mRNA调控研究

• 批准号: 13670511
• 负责人: TSUDA Kinsuke
• 金额: $ 2.24万
• 依托单位: KYOTO UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13670511/
• 关键词: α-glucosidase; Voglivose; Maltase; sucrase; Small intestine; postpraudialplasmaglucose; αグルコシダーゼ

The effect of long-term (6 months) administration of voglibose in a dietary mixture (10 ppm) on intestinal disaccharidase activity was examined in non obese type 2 diabetes model Goto-Kakizaki (GK) rats. The postprandial blood glucose level in voglibose-treated GK rats was significantly lower than in untreated GK rats (190±19 vs. 250±25 mg/dl, P < 0.01; 1 h, 212±23 vs. 256±20, P < 0.05; 2 h), and the activities of maltase, sucrase, and isomaltase remained significantly lower throughout the 6 months of voglibose treatment. The expressions of protein and mRNA of sucrase-isomaltase (SI) complex were significantly higher in voglibose-treated GK rats. Voglibose administration then was stopped after 6 months of treatment. The mRNA level and protein level of the SI complex became normalized during the interruption of drug administration, and disaccharidase activities increased almost to the level of the untreated group 1 month after treatment was stopped. After 1 day of re-administration of the drug, however, disaccharidase activities again became significantly inhibited. These results indicate that voglibose may improve glucose tolerance since it inhibits activities of disaccharidases in spite of increasing the expression of them on intestine, furthermore voglibose may be reversible and reproducible through interruption and re-administration.* 2002 Elsevier Science Ireland Ltd. All rights reserved.

在非肥胖型2型糖尿病模型Goto-Kakizaki(GK)大鼠上，观察了长期(6个月)在混合饮食(10ppm)中给予伏格列波糖对肠道双糖酶活性的影响。伏格列波糖组GK大鼠餐后血糖水平显著低于未治疗组(190±19vs.250±25 mg/dl，P<0.01；1h，212±23vs.256±20，P&lt；0.05；2 h)，麦芽糖酶、蔗糖酶和异麦芽糖酶活性在整个治疗6个月期间持续显著降低。伏格列波糖治疗后GK大鼠蔗糖酶-异麦芽糖酶(SI)复合体的蛋白和mRNA表达明显增加。治疗6个月后停用伏格列波糖。停药1个月后，SI复合体的mRNA水平和蛋白水平恢复正常，双糖酶活性几乎恢复到未用药组水平。然而，在重新给药1天后，双糖酶活性再次受到显著抑制。这些结果表明，伏格列波糖可以改善葡萄糖耐量，因为它抑制了二糖酶的活性，尽管它们在肠道上的表达增加，而且伏格列波糖通过中断和重新给药可能是可逆的和可重现的。*2002爱思唯尔爱尔兰科学有限公司。保留所有权利。

项目成果

K.Yasuda, et al.: "Growth-related changes in skeletal muscle fiber type and insulin resistance in diabetic Otsuka Long -Evance Tokushima Fatty Rats"Acta Histochem. Cytochem. 34(5). 371-382 (2001)

K.Yasuda等人：“糖尿病大冢Long-Evance德岛脂肪大鼠中骨骼肌纤维类型和胰岛素抵抗的生长相关变化”Acta Histochem。

Yasuda K, et al.: "Abnormality in fiber type distribution of soleus and plantaris muscle in non-obese diabetic Goto-Kakizaki rats"Clin Experiment Pharmacol Physiology. 29. 1001-1008 (2002)

Yasuda K 等人：“非肥胖糖尿病 Goto-Kakizaki 大鼠中比目鱼肌和跖肌的纤维类型分布异常”临床实验药理学生理学。

K. Miyawaki, et al.: "Inhibition of gastric inhibitory polypeptide signaling prevents obesity"Nature Med. 8(7). 738-742 (2002)

K. Miyawaki 等人：“抑制胃抑制性多肽信号传导可预防肥胖”Nature Med。

津田 謹輔: "看護のための最新医学講座 29巻 栄養療法・輸液"中山書店. 380 (2002)

津田金介：《最新护理医学课程第 29 卷：营养治疗/输液》中山书店 380 (2002)。

K.Yasuda, et al.: "Normalization of cytoplasmic calcium response in pancreatic beta-cells of spntaneously diabetic GK rat by the treatment with T-1095, a specific inhibitor of renal Na-glucose cotransporters"Horm Metab Res. 34(4). 217-212 (2002)

K.Yasuda 等人：“通过用 T-1095（肾钠-葡萄糖协同转运蛋白的特异性抑制剂）治疗，使自发性糖尿病 GK 大鼠的胰腺 β 细胞中的细胞质钙反应正常化”Horm Metab Res。