Maternal dietary olive oil protects diabetic rat offspring from impaired uterine decidualization

IF 2.5 2区 医学 Q2 DEVELOPMENTAL BIOLOGY Placenta Pub Date : 2026-01-01 Epub Date: 2024-11-21 DOI:10.1016/j.placenta.2024.11.010
Cintia Romina Gatti , Florencia Schibert , Virginia Soledad Taylor , Evangelina Capobianco , Verónica Montero , Romina Higa , Alicia Jawerbaum
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Abstract

Introduction

Maternal diabetes increases the risk of adverse maternal, perinatal and offspring outcomes. This study aimed to address whether alterations in uterine decidualization are programmed in the prepubertal offspring from diabetic rats fed diets enriched or not in extra virgin olive oil (EVOO).

Methods

Control and mild pregestational diabetic female rats (F0) were mated with control males and fed diets enriched or not with 6 % EVOO during pregnancy. Offspring (F1) were evaluated on postnatal day 30, after induction of uterine decidualization (PMSG 50 IU- hCG 50 IU). Signaling pathways involved in decidualization, including prolactin, PPAR and mTOR pathways as well as microRNAs (miRs) regulating these pathways were evaluated by Western blot or qPCR in the decidualized uteri.

Results

The offspring from diabetic rats evidenced reduced prolactin and prolactin receptor levels in the decidualized uteri. Additionally, these tissues showed increased PPARγ levels and reduced levels of its negative regulators miR-19b and miR-155. MiR-21, a microRNA that targets both PPARα and mTOR pathway regulators was reduced, whereas PPARα, PTEN and FOXO1 mRNA levels were increased in the decidualized uteri of the offspring from diabetic rats. The mTOR pathway activity was reduced in the decidualized uteri of the offspring from diabetic rats. Most of the observed alterations were prevented by the EVOO-enriched maternal diet.

Discussion

Impaired pathways relevant to decidualization are programmed in the uteri of prepubertal offspring from diabetic dams, alterations capable of being prevented by maternal diets enriched in EVOO.
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母体饮食中橄榄油可保护糖尿病大鼠后代免受子宫脱个体化损害。
母体糖尿病增加了母体、围产期和后代不良结局的风险。本研究旨在探讨在糖尿病大鼠的青春期前后代中,子宫脱卵化的改变是否与喂食富含或不富含特级初榨橄榄油(EVOO)的饮食有关。方法:将正常、轻度妊娠糖尿病雌性大鼠(F0)与对照雄性大鼠交配,在妊娠期间分别饲喂添加或不添加6% EVOO的饲粮。子代(F1)在产后30天,子宫脱位诱导(PMSG 50 IU- hCG 50 IU)后进行评估。采用Western blot或qPCR方法对去个性化子宫中参与去个性化的信号通路,包括泌乳素、PPAR和mTOR通路以及调节这些通路的microrna (mir)进行评估。结果:糖尿病大鼠后代在去个体化子宫内泌乳素和泌乳素受体水平明显降低。此外,这些组织显示PPARγ水平升高,其负调节因子miR-19b和miR-155水平降低。MiR-21是一种靶向PPARα和mTOR通路调节因子的microRNA,在糖尿病大鼠后代的去个化子宫中降低,而PPARα、PTEN和FOXO1 mRNA水平升高。糖尿病大鼠后代去个体化子宫中mTOR通路活性降低。大多数观察到的改变被富含evoo的母体饮食所阻止。讨论:与去个体化相关的受损通路在糖尿病母亲的青春期前后代的子宫中被编程,这种改变可以通过富含EVOO的母亲饮食来预防。
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来源期刊
Placenta
Placenta 医学-发育生物学
CiteScore
6.30
自引率
10.50%
发文量
391
审稿时长
78 days
期刊介绍: Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.
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