A maternal diet high in carbohydrates causes bradyarrhythmias and changes in heart rate variability in the offspring sex-dependent in mice.

IF 2.7 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Laboratory Animal Research Pub Date : 2024-09-27 DOI:10.1186/s42826-024-00222-6
Rosa Elena Arroyo-Carmona, Yareth Mitre-Velasco, Ygnacio Martinez-Laguna, Julián Torres-Jácome, Alondra Albarado-Ibañez
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Abstract

Background: Maternal obesity prepregnancy, as well as gestational overweight produced by high-sucrose diet, could be evolved to the cardiometabolic diseases in offspring during adulthood. Until then, the cardiometabolic diseases were ignored that have been presented or inherited in the offspring for overnutrition were ignored, depend on gender. We proposed that maternal prepregnancy obesity in CD1 mice, as well as gestational overweight produced by a high sucrose diet, develop to cardiometabolic disease in offspring and even if gender. For detection of the cardiometabolic diseases in a Murine model with a high sucrose diet (HSD), the time series formed by the RR intervals taken from lead I of the ECG has used the corresponding Poincare plot. The heart rate variability was characterized by the standard deviation of width and length SD1, SD2 respectively of the Poincare plot and the SD1/SD2 correlation index in addition was calculated between to gender and body weight.

Results: A maternal diet was based high sucrose diet and produced overweight on progeny in both sexes, but the cardiac arrhythmias depended on gender. Other results were due to the chronic effect of high sucrose diet in offspring with this intrauterine ambiance that contributes to changes in HRV, arrhythmias, and sinus pauses, also these phenomena were observed just in the male mice offspring with high sucrose diet during adulthood.

Conclusions: We propose, that the arrhythmias originated from fetal programming due to the maternal diet in mice model and produced alterations in the offspring female more than in the male, probably due to hormones.

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高碳水化合物的母体饮食会导致小鼠性早熟和后代心率变异性的变化。
背景:母体孕前肥胖以及高蔗糖饮食导致的妊娠超重可能会导致后代成年后患上心脏代谢疾病。在此之前,人们忽视了因营养过剩导致的后代出现或遗传的心脏代谢疾病,这与性别有关。我们提出,CD1 小鼠的母体孕前肥胖以及高蔗糖饮食导致的妊娠超重会发展成后代的心脏代谢疾病,即使性别相同也是如此。为了检测高蔗糖饮食(HSD)小鼠模型中的心脏代谢疾病,使用了相应的 Poincare 图来表示心电图 I 导联 RR 间期所形成的时间序列。心率变异性的特征是波恩卡雷图的宽度和长度的标准偏差 SD1 和 SD2,此外还计算了性别和体重之间的 SD1/SD2 相关指数:结果:以高蔗糖饮食为基础的母体饮食会导致雌雄后代超重,但心律失常取决于性别。其他结果是由于高蔗糖饮食对后代宫内环境的长期影响,导致心率变异、心律失常和窦性停搏的变化,而且这些现象仅在成年期高蔗糖饮食的雄性小鼠后代中观察到:我们认为,在小鼠模型中,心律失常源于母体饮食导致的胎儿编程,在后代中,雌性小鼠比雄性小鼠产生的改变更多,这可能是激素的作用。
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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
32
审稿时长
8 weeks
期刊最新文献
Observation of neutrophil extracellular traps in the development of diabetic nephropathy using diabetic murine models. Hypoxia-inducible factor-1α-deficient adipose-tissue macrophages produce the heat to mediate lipolysis of white adipose tissue through uncoupling protein-1. Correction: Effects of single housing on behavior, corticosterone level and body weight in male and female mice. Effects of single housing on behavior, corticosterone level and body weight in male and female mice. A maternal diet high in carbohydrates causes bradyarrhythmias and changes in heart rate variability in the offspring sex-dependent in mice.
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