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ABSTRACT: Role of the gut microbiota in the increased infant body mass index induced by gestational diabetes mellitus

PROVIDER: PRJNA876126 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21397900.fastq.gz	Fastqsanger.gz
	SRR21397901.fastq.gz	Fastqsanger.gz
	SRR21397902.fastq.gz	Fastqsanger.gz
	SRR21397903.fastq.gz	Fastqsanger.gz
	SRR21397904.fastq.gz	Fastqsanger.gz

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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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Project description:We profiled gene expression in peripheral blood cells from 28 obese patients by microarray analysis and visceral fat accumulation caused the gene expression proliles especially in circadian rhythm, inflammation, oxidative stress, and immune response. Obesity was defined as body mass index (BMI) greater than 25 kg/m2 according to the Japanese criteria and visceral fat area (VFA) was estimated by abdominal bioelectrical impedance analysis. Subjects with type 1 diabetes mellitus, autoimmune diseases, malignant diseases, and infectious diseases were excluded. Patients treated with statin and/or thiazolidinediones were also excluded.

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Project description:Gestational diabetes mellitus (GDM) impacts the maternal or infant microbiome trajectory

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NRF2 deficiency leads to inadequate beta cell adaptation during pregnancy and gestational diabetes

Project description:The late stages of mammalian pregnancy are accompanied by a mild increase in insulin resistance likely due to enhanced glucose demand of the growing fetus. Therefore, as an adaptive process to maintain euglycemia during pregnancy, maternal β-cell mass expands leading to increased insulin release. Defects in functional β-cell adaptive expansion during pregnancy can lead to gestational diabetes mellitus (GDM). While the exact mechanisms that promote GDM are poorly understood, GDM is associated with inadequate functional β-cell mass expansion and with a systematic increase of oxidative stress. Here, we show that NRF2 levels are upregulated in mouse β-cells at gestational day 15 (GD15). Inducible β-cell-specific Nrf2 deleted (βNrf2KO) mice display reduced β-cell proliferation, increased β-cell oxidative stress and lipid peroxidation, compromised β-cell function, and elevated β-cell death, leading to impaired β-cell mass expansion and dysregulated glucose homeostasis towards the end of pregnancy. Importantly, the gestational hormone 17-β-estradiol (E2) increases NRF2 levels, and downregulation of NRF2 suppresses E2-induced protection of β-cells against oxidative stress, suggesting that E2 exerts its antioxidant effects through activation of NRF2 signaling in β-cells. Collectively, these data highlight the critical role of NRF2 in regulating oxidative stress during the adaptive response of β-cells in pregnancy and identify NRF2 as a potential therapeutic target for GDM treatment.

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