父亲肥胖会降低婴儿间充质干细胞线粒体的功能能力。

IF 4.2 2区 医学 Q1 ENDOCRINOLOGY & METABOLISM
Filip Jevtovic, Alex Claiborne, Ericka M Biagioni, David N Collier, James E DeVente, Steven Mouro, Tomoko Kaneko-Tarui, Perrie F O-Tierney-Ginn, Laurie J Goodyear, Joseph A Houmard, Nicholas T Broskey, Linda E May
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引用次数: 0

摘要

除了公认的母体健康对胎儿子宫内发育的影响外,最近的流行病学研究还发现,父亲孕前的代谢健康是影响胎儿代谢程序和后代代谢健康的重要因素;然而,这些适应性背后的机制仍局限于动物模型。为了阐明父亲肥胖(P-OB)对人类婴儿新陈代谢的影响,我们研究了间充质干细胞(MSCs),它们能产生婴儿组织,继续参与成熟组织的维护,并与后代供体的表型相似。在这里,我们评估了超重(体重指数25-30kg/m2)(P-OW)或肥胖(体重指数≥30kg/m2)(P-OB)父亲的婴儿间充质干细胞的线粒体功能能力、含量和胰岛素作用,同时控制了母体宫内环境。与P-OW组相比,P-OB组婴儿间充质干细胞的完整细胞呼吸、OXPHOS和电子传递系统能力较低,与线粒体含量的任何变化无关。此外,各组间的葡萄糖处理、胰岛素作用、脂质含量和氧化作用也相似。重要的是,P-OB 组婴儿的体重身长比更大,其部分原因可能是间充质干细胞代谢功能发生了变化,这种变化先于婴儿的生长轨迹,并因此影响了婴儿的生长轨迹。这些数据表明,P-OB 对婴儿间充质干细胞线粒体有负面影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Paternal obesity decreases infant MSC mitochondrial functional capacity.

Besides the well-recognized influence of maternal health on fetal in utero development, recent epidemiological studies appoint paternal preconception metabolic health as a significant factor in shaping fetal metabolic programming and subsequently offspring metabolic health; however, mechanisms behind these adaptations remain confined to animal models. To elucidate the effects of paternal obesity (P-OB) on infant metabolism in humans, we examined mesenchymal stem cells (MSCs), which give rise to infant tissue, remain involved in mature tissue maintenance, and resemble the phenotype of the offspring donor. Here, we assessed mitochondrial functional capacity, content, and insulin action in MSC from infants of fathers with overweight [body mass index (BMI: 25-30 kg/m2); paternal overweight (P-OW)] or obesity (BMI ≥ 30 kg/m2; P-OB) while controlling for maternal intrauterine environment. Compared with P-OW, infant MSCs in the P-OB group had lower intact cell respiration, OXPHOS, and electron transport system capacity, independent of any changes in mitochondrial content. Furthermore, glucose handling, insulin action, lipid content, and oxidation were similar between groups. Importantly, infants in the P-OB group had a greater weight-to-length ratio, which could be in part due to changes in MSC metabolic functioning, which precedes and, therefore, influences infant growth trajectories. These data suggest that P-OB negatively influences infant MSC mitochondria. ClinicalTrials.gov Identifier: NCT03838146.NEW & NOTEWORTHY Paternal obesity decreases infant mesenchymal stem cell (MSC) basal and maximal respiration. Lower OXPHOS and electron transport system capacity could be explained by lower complex I and IV respiratory capacity but not changes in OXPHOS expression in infant MSC from fathers with obesity. Paternal obesity and altered MSC mitochondrial functional capacity are associated with a greater infant weight-to-length ratio at birth.

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来源期刊
CiteScore
9.80
自引率
0.00%
发文量
98
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Endocrinology and Metabolism publishes original, mechanistic studies on the physiology of endocrine and metabolic systems. Physiological, cellular, and molecular studies in whole animals or humans will be considered. Specific themes include, but are not limited to, mechanisms of hormone and growth factor action; hormonal and nutritional regulation of metabolism, inflammation, microbiome and energy balance; integrative organ cross talk; paracrine and autocrine control of endocrine cells; function and activation of hormone receptors; endocrine or metabolic control of channels, transporters, and membrane function; temporal analysis of hormone secretion and metabolism; and mathematical/kinetic modeling of metabolism. Novel molecular, immunological, or biophysical studies of hormone action are also welcome.
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