饮食诱导的2型糖尿病雌雄小鼠的肾功能和葡萄糖转运。

W T Noonan, R O Banks
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引用次数: 34

摘要

本研究的目的是测量饮食诱导的2型糖尿病雄性和雌性C57BL/6J小鼠的心血管和肾脏功能,包括肾脏葡萄糖转运能力。典型的II型糖尿病小鼠,喂食高脂肪、高简单碳水化合物3个月后出现肥胖(45-65 g)、高血糖(138-259 mg%)和高胰岛素(1.8-15.06 ng/ml);在所有病例中均观察到显著的性别差异。根据清醒小鼠的收缩压测量和麻醉小鼠的动脉血压测量,无论是雄性还是雌性小鼠都没有观察到饮食引起的高血压。高脂高单碳水化合物饲粮雄性小鼠的尿流率、钠、钾、渗透压和蛋白质排泄率均显著高于雌性小鼠(P < 0.05)。然而,饲喂对照饮食的雄性和雌性小鼠在排泄变量上没有差异。fitc -菊粉测定的对照组(0.87 +/- 0.01和0.90 +/- 0.1)和高脂高单碳水化合物饲粮(0.96 +/- 0.1和0.93 +/- 0.2)各组小鼠肾小球滤过率(ml min-1 g kw-1)无显著差异。这些高血糖小鼠也没有血糖。连续3个月或6个月不断给雄性小鼠输注葡萄糖,结果显示所有小鼠的肾阈值为400mg %,远高于本研究中观察到的空腹血浆葡萄糖浓度。因此,C57BL/6J小鼠是研究饮食性肥胖、高血糖和高胰岛素血症的有价值的工具;然而,在本研究的时间框架内,没有明显的高血压或肾功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Renal function and glucose transport in male and female mice with diet-induced type II diabetes mellitus.

The aim of this study was to measure cardiovascular and renal function, including the renal transport capacity for glucose, in male and female C57BL/6J mice with diet-induced Type II diabetes mellitus. Typical of Type II diabetes, mice fed a high-fat, high-simple carbohydrate diet for 3 months were obese (45-65 g), hyperglycemic (138-259 mg%), and hyperinsulinemic (1.8-15.06 ng/ml); significant gender differences were observed in all cases. Based on systolic pressure measurements in conscious mice and arterial blood pressure measurements in anesthetized mice, no diet-induced hypertension was observed in either male or female mice. Urine flow rate, sodium, potassium, osmolar, and protein excretion rates were significantly increased (P < 0.05) in male mice fed the high-fat, high-simple carbohydrate diet compared with female mice fed the same diet. However, no differences in the excretion variables existed between male and female mice fed the control diet. The glomerular filtration rate (ml min-1 g kw-1), determined by FITC-inulin, in male and female mice fed the control diet (0.87 +/- 0.01 and 0.90 +/- 0.1, respectively) and high-fat, high-simple carbohydrate diet (0.96 +/- 0.1 and 0.93 +/- 0.2, respectively) was not different between the groups. These hyperglycemic mice were also not glucosuric. Infusions of progressive amounts of glucose in male mice fed either diet for 3 or 6 months demonstrated that the renal threshold for glucose was 400 mg% for all these mice, well above the fasting plasma glucose concentrations observed in this study. Thus, C57BL/6J mice were valuable tools for studying diet-induced obesity, hyperglycemia, and hyperinsulinemia; however, no hypertension or kidney dysfunction was apparent within the time frame of the current study.

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