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NRF2 Dysregulation Leads to Inadequate Beta-Cell Mass Expansion during Pregnancy and Gestational Diabetes

ABSTRACT: NRF2 Dysregulation Leads to Inadequate Beta-Cell Mass Expansion during Pregnancy and Gestational Diabetes

PROVIDER: PRJNA1221270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR32279369_1.fastq.gz	Fastqsanger.gz
	SRR32279369_2.fastq.gz	Fastqsanger.gz
	SRR32279370_1.fastq.gz	Fastqsanger.gz
	SRR32279370_2.fastq.gz	Fastqsanger.gz

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NRF2 Dysregulation Leads to Inadequate Beta-Cell Mass Expansion during Pregnancy and Gestational Diabetes

Project description:The late stages of the mammalian pregnancy are accompanied with increased insulin resistance due to the increased glucose demand of the growing fetus. Therefore, as a compensatory response to maintain maternal normal blood glucose levels, maternal β-cell mass expands leading to increased insulin release. Defects in β-cell adaptive expansion during pregnancy can lead to gestational diabetes mellitus (GDM). Although the exact mechanisms that promote GDM are poorly understood, GDM strongly associates with impaired β-cell proliferation and with increased levels of oxidative stress. Here, we show that NRF2 levels are upregulated in mouse β-cells at gestational day 15 (GD15) concomitant with increased β-cell proliferation. Inducible β-cell-specific Nrf2 deleted (βNrf2KO) mice display blunted β-cell proliferation, increased β-cell oxidative stress and lipid peroxidation, impaired β-cell function, and elevated β-cell death, leading to attenuated β-cell mass expansion and altered glucose homeostasis towards the end of pregnancy. Importantly, the gestational hormone, 17-β-estradiol (E2), increases NRF2 levels and the downregulation of NRF2 suppresses E2-dependent protection of β-cells against oxidative stress, suggesting that E2 exerts its antioxidant effects through activation of the NRF2 signaling in β-cells. Collectively, these data highlight the importance of NRF2 in the regulation of oxidative stress in the adaptive response of β-cells during pregnancy and identify NRF2 as a potential therapeutic target for GDM treatment.

2025-03-07 | GSE289077 | GEO

Role of microRNAs in compensatory b-cell mass expansion associated with pregnancy and obesity

Project description:We found that in rodents, b-cell mass expansion during pregnancy and obesity is associated with changes in the expression of a group of islet microRNAs. We were able to reproduce in isolated pancreatic islets the decrease of miR-338-3p level observed in gestation and obesity by activating the G-protein coupled estrogen receptor GPR30 and the GLP1 receptor. Blockade of miR-338-3p in b-cells using specific anti-miR molecules mimicked gene expression changes occurring during b-cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. These findings point to a major role for miR-338-3p in compensatory b-cell mass expansion occurring under different insulin resistance states.

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Nrf2 transcript alterations

Project description:WGS and RNA-seq data for Nrf2 study

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Gestational chronodisruption throughout pregnancy impairs adipose tissue physiology in the offspring

Project description:Compelling evidence supports that gestational chronodisruption induces major changes in maternal circadian rhythms, fetal development and that these changes impact adult life at many physiological levels. Using a rat model of chronic photoperiod shifting throughout gestation (CPS), we investigated the detrimental effects of gestational CPS on glucose homeostasis, adipose tissue physiology and metabolism in the adult male offspring. At proteomic level, in CPS adipose tissue, 275 proteins displayed differential expression, compared with LD animals fed with a standard diet. Interestingly, CPS offspring and LD fed with HFD showed 20 proteins in common (2 upregulated 18 downregulated). Based on these common proteins, the IPA analysis found that 2 functional pathways were significantly altered; the network 1 (AKT/ERK) and the network 2 (TNF/IL4).

2021-08-11 | PXD026315 | Pride

Maternal gestational nutrition perturbs offspring sperm epigenome in sheep [BiSulfite-seq]

Project description:There is a growing body of evidence that inadequate maternal nutrition during gestation can have immediate and life-long effects on offspring. However, little is known about the reproductive effects of maternal gestational nutrition in offspring males. Here, using a sheep model of poor maternal nutrition (restricted- or over-feeding) during gestation, we found that poor maternal gestational nutrition does not affect semen characteristics (i.e. volume, sperm concentration, pH, sperm motility, sperm morphology) and scrotal circumference in offspring. However, by evaluating associations between poor maternal gestational nutrition and altered small non-cording RNAs (sncRNAs) and DNA methylation in offspring sperm, we demonstrated that poor maternal gestational nutrition alters sperm sncRNA composition and expression. Whole genome bisulfite sequencing further identified genomic regions with increased or decreased DNA methylation in sperm in response to poor maternal gestational nutrition. These findings imply that maternal diet-induced epigenetic errors can accumulate in sperm to worsen developmental outcomes of future generations.

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Maternal gestational nutrition perturbs offspring sperm epigenome in sheep [ncRNA-seq]

2024-04-04 | GSE225985 | GEO

Differential expression profiles of human primary endothelial cells (HUVECs) from umbilical cords of Gestational Diabetic mothers

Project description:Primary endothelial cells from umbilical cord vein (HUVEC) obtained at delivery from gestational diabetic (GD) women, represent an expedient model for the study of the effects of chronic HG in vivo. In fetal tissues genome-wide epigenetic changes are likely to occur with specific long term and even trans-generational effects. We have utilized this model to study the effects of chronic hyperglycemia on the transcriptome and to verify the presence of specific epigenetic changes associated to chronic HG in vascular cells. HUVEC cells from Umbilical cords of 3 Caucasian Gestational Diabetes women were compared with HUVEC cells from umbilical of from 3 Caucasian non diabetic women matching for age and Body Mass Index. [sample collection] Umbilical cords were obtained from 3 Caucasian Gestational diabetes women (diagnosed not later than 28 th gestational week - gw) and from 3 Caucasian non diabetic women matching for age and Body Mass Index (BMI). All pregnants signed an informed consent. All donors were normotensive, and underwent a 100 g 3 hours Oral Glucose Tolerance Test (OGTT) between the 24 -34th gw. Each woman performed a 7 points-blood glucose monitoring on 3 days at week 34 -36th gw.

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NRF2 Is Required for Neonatal Beta-Cell Growth by Maintaining Redox Balance and Promoting Mitochondrial Biogenesis and Function

Project description:Due to the limited expression of several antioxidant enzymes, β-cells are highly vulnerable to high ROS levels, which can lead to the reduction of functional β-cell mass. During early postnatal ages, both human and rodent β-cells go through a burst of proliferation that quickly declines with age. Here we discovered that the expression of the master antioxidant regulator, Nrf2, is increased during this postnatal burst of β-cell proliferation in humans. Additionally, data from β-cell specific Nrf2 deletion in mice demonstrated that Nrf2 is required for β-cell proliferation, β-cell survival, β-cell identity and β-cell mass expansion at early stages of life. Daily administration of antioxidant NAC to newborn mice showed that Nrf2 mechanism of action strongly relies on maintaining normal redox balance. Interestingly, RNAseq of islets isolated from β-cell specific Nrf2 deleted mice suggests that Nrf2 regulates neonatal β-cell proliferation by promoting mitochondrial ATP synthesis. Our study highlights Nrf2 as an essential transcription factor for maintaining redox balance as well as mitochondrial biogenesis and function to support neonatal β-cell growth and for maintaining functional β-cell mass in adulthood under metabolic stress.

2023-12-19 | GSE242718 | GEO

Maternal whole blood expression changes with gestational age and labor in normal pregnancy [array]

Project description:Maternal plasama colected longitudinally were profiled using Affymetrix Human Transcriptome Arrays to evaluate changes with gestational age and with labor in normal pregnancy.

2019-02-04 | GSE113809 | GEO

Maternal whole blood expression changes with gestational age in normal pregnancy by Human Transcriptome Arrays

Project description:Maternal plasama colected longitudinally were profiled using Affymetrix Human Transcriptome Arrays to evaluate changes with gestational age.

2019-12-17 | GSE121974 | GEO

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