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高糖饮食对肥胖小鼠(C57BL/6J obob)空肠中蔗糖酶和乳糖酶活性的影响。

Effect of a high-dextrose diet on sucrase and lactase activity in jejunum of obese mice (C57BL/6J obob).

作者信息

Flores C A, Bezerra J, Goda T, Bustamante S, MacDonald M P, Kaplan M, Koldovský O

出版信息

J Am Coll Nutr. 1986;5(6):565-75. doi: 10.1080/07315724.1986.10720157.

Abstract

The activities of intestinal disaccharidases are known to be responsive to changes in the dietary intake of carbohydrates in the adult rat. Little is known, however, regarding the activities of these enzymes in obese subjects and how they are affected by differing carbohydrate intakes. To evaluate the effect of carbohydrate intake on the activity of intestinal disaccharidases in obesity, we used the genetically obese mouse C57BL/6J obob as an experimental model. Representing an example of early-onset obesity and mature-onset diabetes, this animal is characteristically hyperinsulinemic and hyperglycemic. Groups of obese mice and lean littermates were fed for 7 weeks equal amounts of either high-dextrose or low-dextrose isoenergetic diets. Sucrase, maltase, and lactase activities were measured on intestinal homogenates from the proximal and middle portions of the jejunoileum (upper and lower jejunum). Results were expressed as activity per tissue protein as well as total activity. Obese mice were found to have consistently greater total activity of both sucrase and maltase than their lean littermates, mostly as a result of increased intestinal size. Total lactase activity, however, was similar in the upper jejunum in both obese and lean mice, largely related to a decreased specific activity in obese mice. All mice fed the high-dextrose diet had significantly increased total activity of all disaccharidases studied when compared to the low-dextrose-fed animals, except for the lactase activity in the lower jejunum, where no differences were found in either group. Increases in activity related to high carbohydrate intake were a result of increases in specific activity.

摘要

已知成年大鼠肠道双糖酶的活性对碳水化合物饮食摄入量的变化有反应。然而,对于肥胖受试者中这些酶的活性以及它们如何受到不同碳水化合物摄入量的影响,人们了解甚少。为了评估碳水化合物摄入量对肥胖状态下肠道双糖酶活性的影响,我们使用遗传性肥胖小鼠C57BL/6J obob作为实验模型。这种动物代表早发性肥胖和成年发病型糖尿病的一个例子,其特征是高胰岛素血症和高血糖症。将肥胖小鼠组和瘦的同窝小鼠分别喂食等量的高葡萄糖或低葡萄糖等能量饮食7周。对空肠回肠近端和中部(空肠上段和下段)的肠道匀浆进行蔗糖酶、麦芽糖酶和乳糖酶活性测定。结果以每组织蛋白的活性以及总活性表示。发现肥胖小鼠的蔗糖酶和麦芽糖酶总活性始终高于它们瘦的同窝小鼠,这主要是由于肠道大小增加所致。然而,肥胖小鼠和瘦小鼠空肠上段的乳糖酶总活性相似,这在很大程度上与肥胖小鼠中比活性降低有关。与喂食低葡萄糖饮食的动物相比,所有喂食高葡萄糖饮食的小鼠所研究的所有双糖酶的总活性均显著增加,但空肠下段的乳糖酶活性除外,两组在该部位均未发现差异。与高碳水化合物摄入相关的活性增加是比活性增加的结果。

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