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大豆分离肽饮食可促进II型糖尿病小鼠餐后碳水化合物氧化和能量消耗。

A soybean peptide isolate diet promotes postprandial carbohydrate oxidation and energy expenditure in type II diabetic mice.

作者信息

Ishihara Kengo, Oyaizu Shinichi, Fukuchi Yoshiko, Mizunoya Wataru, Segawa Kikumi, Takahashi Miki, Mita Yukiko, Fukuya Yoko, Fushiki Tohru, Yasumoto Kyoden

机构信息

Department of Food and Nutrition, School of Life Studies, Sugiyama Jogakuen University, Nagoya 464-8662, Japan.

出版信息

J Nutr. 2003 Mar;133(3):752-7. doi: 10.1093/jn/133.3.752.

Abstract

The aim of the present study was to determine the effects of dietary proteins on the oxidation of dietary carbohydrate and lipids in type II diabetic mice. KK-A(y) strain mice were provided free access to a high fat diet (30% of energy as fat) for an initial 4-wk period to induce diabetes. To reduce body weight gain, the mice were subsequently fed restrictive isoenergetic and isonitrogenous diets (35% of energy as protein and 5% as fat) based on either casein or soy protein isolate hydrolysate (SPI-H) for 4 wk. To measure exogenous carbohydrate and lipid oxidation, the mice were fed a diet containing (13)C-glucose or (13)C-triolein while they were in a respiratory chamber for 72 h. Postprandial energy expenditure was higher in the SPI-H than in the casein group; this difference was due to an increase in postprandial exogenous and endogenous carbohydrate oxidation. There were no differences in 24-h energy expenditure between dietary groups. Oxidation of exogenous carbohydrate tended to be higher (P = 0.054) in the SPI-H group during the 24 h of measurement. Fecal excretion of (13)C-glucose was lower but the excretion of lipid was higher in mice fed the SPI-H diet than in casein-fed mice. These results indicate that in type II diabetic mice, dietary SPI-H not only inhibits the absorption of dietary lipids and increases the absorption of dietary carbohydrates but also augments postprandial energy expenditure, which is accompanied by a postprandial increase in oxidation of dietary carbohydrates.

摘要

本研究的目的是确定膳食蛋白质对II型糖尿病小鼠膳食碳水化合物和脂质氧化的影响。最初4周,给予KK-A(y)品系小鼠自由摄取高脂肪饮食(脂肪提供30%的能量)以诱导糖尿病。为了减少体重增加,随后给小鼠喂食基于酪蛋白或大豆分离蛋白水解物(SPI-H)的限制性等能量和等氮饮食(蛋白质提供35%的能量,脂肪提供5%的能量),持续4周。为了测量外源性碳水化合物和脂质氧化,在小鼠处于呼吸室的72小时内,给它们喂食含有(13)C-葡萄糖或(13)C-三油精的饮食。餐后能量消耗在SPI-H组高于酪蛋白组;这种差异是由于餐后外源性和内源性碳水化合物氧化增加所致。各饮食组之间24小时能量消耗没有差异。在24小时测量期间,SPI-H组外源性碳水化合物的氧化倾向于更高(P = 0.054)。喂食SPI-H饮食的小鼠粪便中(13)C-葡萄糖的排泄较低,但脂质排泄高于喂食酪蛋白的小鼠。这些结果表明,在II型糖尿病小鼠中,膳食SPI-H不仅抑制膳食脂质的吸收并增加膳食碳水化合物的吸收,还增加餐后能量消耗,同时伴有餐后膳食碳水化合物氧化增加。

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