母体高血糖及其对人类后代的长期影响。

IF 2 4区 医学 Q3 PHYSIOLOGY Journal of Physiology and Pharmacology Pub Date : 2024-10-01 Epub Date: 2024-12-04 DOI:10.26402/jpp.2024.5.01
A Gladych-Macioszek, K Ozegowska, S Radzicka-Mularczyk, K Tobola-Wrobel, E Wender-Ozegowska
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引用次数: 0

摘要

孕妇患糖尿病被认为是胎儿发育过程中的一个因素,不仅会导致怀孕期间的几种并发症,而且还会增加晚年患慢性病的风险,并对后代的健康产生持久影响。动物模型在建立产前母体糖尿病暴露与后代持久健康之间的明确因果关系方面发挥了作用,有助于控制可能扭曲结果的变量。本研究旨在系统分析与母亲糖尿病相关的长期后代并发症,从人类和动物研究中获得见解。通过对妊娠期高血糖影响胎儿发育的机制的详细分析,扩大了关于预防和治疗妊娠期高血糖的科学研究可能的新方向的知识。
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Maternal hyperglycemia and long-term consequences for human offspring.

Exposure to maternal diabetes is considered one of the factors during foetal development, leading not only to several complications during pregnancy but also to an increased risk of chronic diseases in later life and exerting a lasting impact on the health of offspring. Animal models play a role in establishing a clear cause-and-effect relationship between prenatal exposure to maternal diabetes and the enduring well-being of offspring, helping to control for variables that could distort the results. This study aims to systematically analysis long-term offspring complications associated with maternal diabetes, drawing insights from both human and animal studies. Analysis expands knowledge about possible new directions of scientific research concerning the prevention and treatment of hyperglycemia in pregnancy through a detailed analysis of the mechanisms of its influence on fetal development.

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来源期刊
CiteScore
4.00
自引率
22.70%
发文量
0
审稿时长
6-12 weeks
期刊介绍: Journal of Physiology and Pharmacology publishes papers which fall within the range of basic and applied physiology, pathophysiology and pharmacology. The papers should illustrate new physiological or pharmacological mechanisms at the level of the cell membrane, single cells, tissues or organs. Clinical studies, that are of fundamental importance and have a direct bearing on the pathophysiology will also be considered. Letters related to articles published in The Journal with topics of general professional interest are welcome.
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