Suppr超能文献

产后高脂饮食对后代母体肥胖的肾脏影响起主导作用。

The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet.

作者信息

Glastras Sarah J, Chen Hui, Tsang Michael, Teh Rachel, McGrath Rachel T, Zaky Amgad, Chen Jason, Wong Muh Geot, Pollock Carol A, Saad Sonia

机构信息

Department of Medicine, Kolling Institute, University of Sydney, Sydney, Australia.

Department of Diabetes, Endocrinology and Metabolism, Royal North Shore Hospital, St Leonards, NSW, Australia.

出版信息

PLoS One. 2017 Feb 22;12(2):e0172644. doi: 10.1371/journal.pone.0172644. eCollection 2017.

Abstract

AIMS/HYPOTHESIS: Developmental programming induced by maternal obesity influences the development of chronic disease in offspring. In the present study, we aimed to determine whether maternal obesity exaggerates obesity-related kidney disease.

METHODS

Female C57BL/6 mice were fed high-fat diet (HFD) for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow or HFD. At postnatal Week 8, HFD-fed offspring were administered one dose streptozotocin (STZ, 100 mg/kg i.p.) or vehicle control. Metabolic parameters and renal functional and structural changes were observed at postnatal Week 32.

RESULTS

HFD-fed offspring had increased adiposity, glucose intolerance and hyperlipidaemia, associated with increased albuminuria and serum creatinine levels. Their kidneys displayed structural changes with increased levels of fibrotic, inflammatory and oxidative stress markers. STZ administration did not potentiate the renal effects of HFD. Though maternal obesity had a sustained effect on serum creatinine and oxidative stress markers in lean offspring, the renal consequences of maternal obesity were overwhelmed by the powerful effect of diet-induced obesity.

CONCLUSION

Maternal obesity portends significant risks for metabolic and renal health in adult offspring. However, diet-induced obesity is an overwhelming and potent stimulus for the development of CKD that is not potentiated by maternal obesity.

摘要

目的/假设:母体肥胖引起的发育编程会影响后代慢性疾病的发展。在本研究中,我们旨在确定母体肥胖是否会加剧与肥胖相关的肾脏疾病。

方法

雌性C57BL/6小鼠在交配前、妊娠期和哺乳期喂食高脂饮食(HFD)六周。雄性后代断奶后喂食正常饲料或HFD。在出生后第8周,给喂食HFD的后代腹腔注射一剂链脲佐菌素(STZ,100 mg/kg)或给予载体对照。在出生后第32周观察代谢参数以及肾脏功能和结构的变化。

结果

喂食HFD的后代肥胖增加、葡萄糖耐量降低和血脂异常,伴有蛋白尿和血清肌酐水平升高。它们的肾脏显示出结构变化,纤维化、炎症和氧化应激标志物水平升高。给予STZ并未增强HFD对肾脏的影响。尽管母体肥胖对瘦后代的血清肌酐和氧化应激标志物有持续影响,但饮食诱导的肥胖的强大作用掩盖了母体肥胖对肾脏的影响。

结论

母体肥胖预示着成年后代代谢和肾脏健康的重大风险。然而,饮食诱导的肥胖是慢性肾脏病发展的一个压倒性且强大的刺激因素,母体肥胖不会增强这种刺激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffff/5321436/5516921fef32/pone.0172644.g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验