Department of Human Physiology, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, X54001, South Africa.
Department of Human Physiology, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Room E2 401, Westville, South Africa.
BMC Cardiovasc Disord. 2022 Aug 2;22(1):350. doi: 10.1186/s12872-022-02758-8.
Hyperglycaemia is known to result in oxidative stress tissue injury and dysfunction. Interestingly, studies have reported hepatic and renal oxidative stress injury during prediabetes; however, any injury to the myocardium during prediabetes has not been investigated. Hence this study aims to assess changes in the myocardial tissue in an HFHC diet-induced model of prediabetes.
Male Sprague Dawley rats were randomly grouped into non-prediabetes and prediabetes (n = 6 in each group) and consumed a standard rat chow or fed a high-fat-high-carbohydrate diet respectively for a 20-week prediabetes induction period. Post induction, prediabetes was confirmed using the ADA criteria. Aldose reductase, NADH oxidase 1, superoxide dismutase, glutathione peroxide, cardiac troponins were analysed in cardiac tissue homogenate using specific ELISA kits. Lipid peroxidation was estimated by determining the concentration of malondialdehyde in the heart tissue homogenate according to the previously described protocol. Myocardial tissue sections were stained with H&E stain and analysed using Leica microsystem. All data were expressed as means ± SEM. Statistical comparisons were performed with Graph Pad instat Software using the Student's two-sided t-test. Pearson correlation coefficient was calculated to assess the association. Value of p < 0.05 was considered statistically significant.
The prediabetes group showed a markedly high oxidative stress as indicated by significantly increased NADH oxidase 1 and malondialdehyde while superoxide dismutase and glutathione peroxide were decreased compared to non-prediabetes group. There was no statistical difference between cardiac troponin I and T in the non-prediabetes and prediabetes groups. Cardiac troponins had a weak positive association with glycated haemoglobin.
The findings of this study demonstrate that prediabetes is associated with myocardial injury through oxidative stress. Future studies are to investigate cardiac contractile function and include more cardiac biomarkers.
高血糖会导致氧化应激、组织损伤和功能障碍。有趣的是，研究报道了在糖尿病前期出现肝和肾的氧化应激损伤；然而，糖尿病前期是否对心肌造成损伤尚未得到研究。因此，本研究旨在评估 HFHC 饮食诱导的糖尿病前期模型中心肌组织的变化。
雄性 Sprague Dawley 大鼠被随机分为非糖尿病前期和糖尿病前期组（每组 6 只），分别给予标准大鼠饲料或高脂肪高碳水化合物饮食喂养 20 周诱导糖尿病前期。诱导后，根据 ADA 标准确认糖尿病前期。使用特定的 ELISA 试剂盒分析心脏组织匀浆中的醛糖还原酶、NADH 氧化酶 1、超氧化物歧化酶、谷胱甘肽过氧化物酶和心肌肌钙蛋白。根据先前描述的方案，通过测定心脏组织匀浆中丙二醛的浓度来估计脂质过氧化。用 H&E 染色对心肌组织切片进行染色，并使用 Leica 显微镜系统进行分析。所有数据均表示为平均值±SEM。使用 Graph Pad instat 软件的学生双侧 t 检验进行统计比较。计算 Pearson 相关系数以评估相关性。p 值<0.05 被认为具有统计学意义。
糖尿病前期组的氧化应激明显升高，NADH 氧化酶 1 和丙二醛显著增加，而超氧化物歧化酶和谷胱甘肽过氧化物酶则降低，与非糖尿病前期组相比差异有统计学意义。非糖尿病前期组和糖尿病前期组的心肌肌钙蛋白 I 和 T 无统计学差异。心肌肌钙蛋白与糖化血红蛋白呈弱正相关。
本研究结果表明，糖尿病前期与氧化应激引起的心肌损伤有关。未来的研究将调查心脏收缩功能并包括更多的心脏生物标志物。
