Kanasaki Akane, Iida Tetsuo, Murao Koji, Shirouchi Bungo, Sato Masao
Research and Development, Matsutani Chemical Industry Co., Ltd., 5-3 Kita-Itami, Itami, Hyogo, 664-8508, Japan.
Division of Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa, 761-0793, Japan.
Cytotechnology. 2020 Apr;72(2):295-301. doi: 10.1007/s10616-020-00378-8. Epub 2020 Feb 21.
D-Allulose, a C-3 epimer of D-fructose, is a rare sugar and a non-caloric sweetener. D-Allulose is reported to have several health benefits, such as suppressing a rise in postprandial glucose levels and preventing fat accumulation in rodents and humans. Additionally, low HDL-cholesterol levels post-D-allulose feeding were observed in humans but it is unclear how D-allulose decreased HDL-cholesterol levels. It is necessary to research the mechanism of HDL-cholesterol reduction by D-allulose ingestion because low HDL-cholesterol levels are known to associate with increased atherosclerosis risk. We therefore investigated the mechanism by which D-allulose lowers HDL-cholesterol using rat's primary hepatocytes. Sprague Dawley rats were fed an AIN-93G based diet containing 3% D-allulose for 2 weeks. Thereafter, primary hepatocytes were isolated by perfusion of collagenase. We measured the ability of HDL-cholesterol uptake in hepatocytes and the protein levels of scavenger receptor class B type 1 (SR-B1) as a HDL-cholesterol receptor. D-Allulose enhanced hepatocyte uptake of HDL-cholesterol, with a concurrent increase in hepatic SR-B1 protein levels. The results suggest that D-allulose enhances HDL-cholesterol uptake into the liver by increasing SR-B1 expression. It is estimated that HDL-cholesterol levels decreased accordingly. Since SR-B1 overexpression would decrease HDL-cholesterol levels, reportedly preventing atherosclerosis development, D-allulose could be a useful sweetener for atherosclerosis prevention.
D-阿洛酮糖是D-果糖的C-3差向异构体，是一种稀有糖和无热量甜味剂。据报道，D-阿洛酮糖具有多种健康益处，例如抑制餐后血糖水平升高以及防止啮齿动物和人类体内脂肪堆积。此外，在人类中观察到喂食D-阿洛酮糖后高密度脂蛋白胆固醇（HDL-胆固醇）水平降低，但尚不清楚D-阿洛酮糖如何降低HDL-胆固醇水平。由于已知HDL-胆固醇水平低与动脉粥样硬化风险增加有关，因此有必要研究摄入D-阿洛酮糖降低HDL-胆固醇的机制。因此，我们使用大鼠原代肝细胞研究了D-阿洛酮糖降低HDL-胆固醇的机制。将斯普拉格·道利大鼠喂食含3%D-阿洛酮糖的基于AIN-93G的饮食2周。此后，通过灌注胶原酶分离原代肝细胞。我们测量了肝细胞摄取HDL-胆固醇的能力以及作为HDL-胆固醇受体的B1型清道夫受体（SR-B1）的蛋白质水平。D-阿洛酮糖增强了肝细胞对HDL-胆固醇的摄取，同时肝脏SR-B1蛋白水平增加。结果表明，D-阿洛酮糖通过增加SR-B1表达增强了肝脏对HDL-胆固醇的摄取。据估计，HDL-胆固醇水平相应降低。由于SR-B1过表达会降低HDL-胆固醇水平，据报道可预防动脉粥样硬化发展，因此D-阿洛酮糖可能是预防动脉粥样硬化的有用甜味剂。
