Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Department of Veterinary Biosciences and Public Health, Faculty of Veterinary Medicine, Chiang Mai University, Chiang Mai, 50100, Thailand.
Eur J Nutr. 2021 Jun;60(4):2047-2061. doi: 10.1007/s00394-020-02394-y. Epub 2020 Oct 3.
Obesity-induced insulin resistant is associated with cardiovascular diseases via impairing cardiac mitochondria. Recently, D-allulose could protect β-islets and improve insulin resistance. However, the effects of D-allulose on the heart and cardiac mitochondrial function under obesity-induced insulin-resistant condition has not been investigated. In this study, we aimed to investigate the effects of D-allulose on metabolic parameters, cardiac function, heart rate variability (HRV), cardiac mitochondrial function, and apoptosis in the heart of obesity-induced insulin-resistant rats induced by chronic high fat diet consumption.
Male Wistar rats (n = 24) received a normal fat diet (ND) or high fat diet (HFD) for 12 weeks. Then, HFD group was randomly divided into three subgroups to receive (1) HFD with distilled water, (2) HFD with 3% D-allulose 1.9 g/ kg·BW/ day (HFR), and (3) HFD with metformin 300 mg/kg·BW/ day (HFM) by diluted in drinking water daily for 12 weeks. At week 24, proposed study parameters were investigated.
Chronic HFD consumption induced obesity-induced insulin resistant in rats and high fat diet impaired cardiac function and HRV. HFR rats had improved insulin sensitivity as indicated by decreasing HOMA index, plasma insulin, whereas HFM decreased body weight, visceral fat, plasma cholesterol, and plasma LDL. HFR and HFM provided similar efficacy in improving HRV and attenuating cardiac mitochondrial dysfunction, leading to improved cardiac function.
Even though this is the first investigation of the D-allulose impact on the heart with a relatively small sample size, it clearly demonstrated a beneficial effect on the heart. D-allulose exerted a therapeutic effect on metabolic parameters except for body weight and lipid profiles and provided cardioprotective effects similar to metformin via attenuating cardiac mitochondrial function in obesity-induced insulin-resistant rats.
肥胖引起的胰岛素抵抗通过损害心脏线粒体与心血管疾病有关。最近，D-阿洛酮糖可以保护β胰岛并改善胰岛素抵抗。然而，在肥胖引起的胰岛素抵抗情况下，D-阿洛酮糖对心脏和心脏线粒体功能的影响尚未得到研究。在这项研究中，我们旨在研究 D-阿洛酮糖对慢性高脂肪饮食诱导肥胖诱导的胰岛素抵抗大鼠代谢参数、心脏功能、心率变异性（HRV）、心脏线粒体功能和心脏细胞凋亡的影响。
雄性 Wistar 大鼠（n=24）接受正常脂肪饮食（ND）或高脂肪饮食（HFD）12 周。然后，HFD 组随机分为三组，分别给予（1）HFD 加蒸馏水，（2）HFD 加 3%D-阿洛酮糖 1.9g/kg·BW/天（HFR），和（3）HFD 加二甲双胍 300mg/kg·BW/天（HFM），每日通过饮用水稀释，持续 12 周。在第 24 周，研究了提出的研究参数。
慢性 HFD 摄入导致大鼠肥胖诱导的胰岛素抵抗，高脂肪饮食损害心脏功能和 HRV。HFR 大鼠的胰岛素敏感性降低，HOMA 指数、血浆胰岛素降低，而 HFM 降低体重、内脏脂肪、血浆胆固醇和 LDL。HFR 和 HFM 在改善 HRV 和减轻心脏线粒体功能障碍方面提供了相似的疗效，从而改善了心脏功能。
尽管这是首次在肥胖诱导的胰岛素抵抗大鼠中研究 D-阿洛酮糖对心脏的影响，但它清楚地表明了对心脏的有益作用。D-阿洛酮糖除了体重和脂质谱外，对代谢参数也有治疗作用，并通过减轻肥胖诱导的胰岛素抵抗大鼠心脏线粒体功能来发挥与二甲双胍相似的心脏保护作用。
