Yagi Takakazu, Ataka Koji, Cheng Kai-Chun, Suzuki Hajime, Ogata Keizaburo, Yoshizaki Yumiko, Takamine Kazunori, Kato Ikuo, Miyawaki Shouichi, Inui Akio, Asakawa Akihiro
Department of Oral Health, Kobe-Tokiwa Junior College, Kobe, Japan.
Department of Orthodontics and Dentofacial Orthopedics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Food Nutr Res. 2020 Oct 8;64. doi: 10.29219/fnr.v64.4226. eCollection 2020.
Red rice (RRK), prepared by growing species on steamed rice, has been reported to lower blood glucose levels in diabetic animal models. However, the action mechanism is not yet completely understood.
The objective of this study was to examine the mechanism underlying the hypoglycemic action of RRK extract in two diabetic animal models: the insulin-deficiency mice, where the insulin deficiency was induced by streptozotocin (STZ), and insulin-resistance mice, where the insulin resistance was induced by a high-fat diet (HFD).
Low (12.5 mg/kg body weight [BW]) and high (50.0 mg/kg BW) doses of RRK extract were orally administered to the mice for 10 successive days (0.25 mL/day/mouse). The protein expression levels of glucose transporter type 4 (GLUT4) in the skeletal muscle and glucose transporter type 2 (GLUT2) in the liver were measured. Blood glucose (BG) levels of STZ-treated mice in insulin tolerance test (ITT) and BG and insulin levels of HFD-fed mice in intraperitoneal glucose tolerance test (IPGTT) were investigated.
In the STZ-treated mice, oral administration of RRK extract lowered BG levels and food intake but increased plasma 1,5-anhydroglucitol level. Moreover, the RRK extract lowered the BG levels of STZ-treated mice as measured by ITT. In the HFD-fed mice, we confirmed that the orally administered RRK extract lowered the BG and the homeostasis model assessment index for insulin resistance. Furthermore, the RRK extract lowered the BG and insulin levels of HFD-fed mice in IPGTT. Regarding the protein levels of GLUT, the orally administered RRK extract increased the GLUT4 level in the skeletal muscle; however, the RRK extract did not alter the GLUT2 level in the liver of either the STZ-treated or the HFD-fed mice.
Our study demonstrates that RRK extract can improve impaired glucose tolerance in mouse models of diabetes by enhancing GLUT4 expression in skeletal muscle.
These results suggest that RRK extract could potentially be a functional food for the treatment of diabetes mellitus.
红米(RRK)是通过在蒸熟的大米上种植菌种制备而成,据报道其可降低糖尿病动物模型的血糖水平。然而,其作用机制尚未完全明确。
本研究旨在探讨RRK提取物在两种糖尿病动物模型中的降血糖作用机制:一是链脲佐菌素(STZ)诱导胰岛素缺乏的小鼠,二是高脂饮食(HFD)诱导胰岛素抵抗的小鼠。
将低剂量(12.5毫克/千克体重[BW])和高剂量(50.0毫克/千克BW)的RRK提取物连续10天口服给予小鼠(0.25毫升/天/只)。检测骨骼肌中葡萄糖转运蛋白4(GLUT4)和肝脏中葡萄糖转运蛋白2(GLUT2)的蛋白表达水平。研究STZ处理小鼠在胰岛素耐量试验(ITT)中的血糖(BG)水平,以及HFD喂养小鼠在腹腔葡萄糖耐量试验(IPGTT)中的BG和胰岛素水平。
在STZ处理的小鼠中,口服RRK提取物可降低BG水平和食物摄入量,但增加血浆1,5-脱水葡萄糖醇水平。此外,通过ITT测量,RRK提取物降低了STZ处理小鼠的BG水平。在HFD喂养的小鼠中,我们证实口服RRK提取物可降低BG和胰岛素抵抗的稳态模型评估指数。此外,RRK提取物降低了HFD喂养小鼠在IPGTT中的BG和胰岛素水平。关于GLUT的蛋白水平,口服RRK提取物可增加骨骼肌中的GLUT4水平;然而,RRK提取物并未改变STZ处理或HFD喂养小鼠肝脏中的GLUT2水平。
我们的研究表明,RRK提取物可通过增强骨骼肌中GLUT4的表达来改善糖尿病小鼠模型受损的葡萄糖耐量。
这些结果表明,RRK提取物可能是一种治疗糖尿病的功能性食品。