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The impact of maternal diet on endocrine islet progenitor cells in mice

ABSTRACT: The goal of this study is to examine how altering maternal diet, including poor- or over-nutrition, impacts the gene expression levels in islet progenitors, including those cells that have not been committed to the endocrine fate and those having committed to it. At present, we will determine the gene expression changes in these progenitors.

ORGANISM(S): Mus musculus

PROVIDER: GSE254702 | GEO | 2025/01/31

REPOSITORIES: GEO

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Endocrine islet beta-cell subtypes with differential function are derived from biochemically distinct embryonic endocrine islet progenitors that are regulated by maternal nutrients

Project description:Endocrine islet beta cells comprise heterogenous cell subsets. Yet the origin, stability, and physiological significance of these subsets remain largely unknown. Using combinatorial cell lineage tracing, scRNA-seq, and DNA methylation analysis, we show here that embryonic islet progenitors with differential gene expression and DNA methylation produce stable beta-cell subtypes of different function and viability in adult mice. Differentially expressed genes, including the Myt transcription factors, voltage-gated channels, and Ca2+-sensor synaptotagmins, contribute to the functional differences of these subtypes. Maternal overnutrition, a major diabetes risk factor, reduces the proportion of endocrine progenitors of the better-functionality beta-cell subtype. Intriguingly, the gene signature that defines mouse beta-cell subtypes can reliably divide human cells into two populations, with the proportion of better-functionality beta cells reduced in diabetic donors. These results establish that some beta-cell subtypes are determined via DNA methylation in embryonic islet progenitors, which is regulated by diabetes-causing maternal factors. The implication is that modulating DNA methylation in islet progenitors can be explored to improve beta-cell function in the prevention and therapy of diabetes.

2025-02-01 | GSE254955 | GEO

Endocrine islet beta-cell subtypes with differential function are derived from biochemically distinct embryonic endocrine islet progenitors that are regulated by maternal nutrients

Project description:Endocrine islet beta-cell subtypes with differential function are derived from biochemically distinct embryonic endocrine islet progenitors that are regulated by maternal nutrients

| PRJNA1072694 | ENA

The impact of maternal diet on endocrine islet progenitor cells in mice

Project description:The impact of maternal diet on endocrine islet progenitor cells in mice

| PRJNA1071543 | ENA

Robust Differentiation of Islet Progenitors into Functional Insulin-secreting Cells by Suppression of Key Transcription Regulators

Project description:Gene profiling revealed that differentiation was accompanied by suppression of a range of transcription regulator genes typical of islet progenitor cells. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control.

2013-11-01 | E-GEOD-51944 | biostudies-arrayexpress

Circulating Metabolites in Progression to Islet Autoimmunity and Type 1 Diabetes

Project description:<h4><strong>AIMS/HYPOTHESIS: </strong>Metabolic dysregulation may precede the onset of type 1 diabetes. However, these metabolic disturbances and their specific role in disease initiation remain poorly understood. In this study, we examined whether children who progress to type 1 diabetes have a circulatory polar metabolite profile distinct from that of children who later progress to islet autoimmunity but not type 1 diabetes and a matched control group.</h4><h4><strong>METHODS: </strong>We analysed polar metabolites from 415 longitudinal plasma samples in a prospective cohort of children in three study groups: those who progressed to type 1 diabetes; those who seroconverted to one islet autoantibody but not to type 1 diabetes; and an antibody-negative control group. Metabolites were measured using two-dimensional GC high-speed time of flight MS.</h4><h4><strong>RESULTS: </strong>In early infancy, progression to type 1 diabetes was associated with downregulated amino acids, sugar derivatives and fatty acids, including catabolites of microbial origin, compared with the control group. Methionine remained persistently upregulated in those progressing to type 1 diabetes compared with the control group and those who seroconverted to one islet autoantibody. The appearance of islet autoantibodies was associated with decreased glutamic and aspartic acids.</h4><h4><strong>CONCLUSIONS/INTERPRETATION: </strong>Our findings suggest that children who progress to type 1 diabetes have a unique metabolic profile, which is, however, altered with the appearance of islet autoantibodies. Our findings may assist with early prediction of the disease.</h4>

2022-01-19 | MTBLS802 | MetaboLights

H3K4 trimethylation is required for postnatal pancreatic endocrine cell functional maturation

Project description:During pancreas development, endocrine progenitors differentiate into the islet-cell subtypes, which undergo further functional maturation in postnatal islet development. In islet b-cells, genes involved in glucose-stimulated insulin secretion are activated and glucose exposure increases the insulin response as b-cells mature. Here, we investigated the role of H3K4 trimethylation in endocrine cell differentiation and functional maturation by disrupting TrxG complex histone methyltransferase activity in mouse endocrine progenitors. In the embryo, genetic inactivation of TrxG component Dpy30 in NEUROG3+ cells did not affect the number of endocrine progenitors or endocrine cell differentiation. H3K4 trimethylation was progressively lost in postnatal islets and the mice displayed elevated non-fasting and fasting glycemia, as well as impaired glucose tolerance by postnatal day 24. Although postnatal endocrine cell proportions were equivalent to controls, islet RNA-sequencing revealed a downregulation of genes involved in glucose-stimulated insulin secretion and an upregulation of immature b-cell genes. Comparison of histone modification enrichment profiles in NEUROG3+ endocrine progenitors and mature islets suggested that genes downregulated by loss of H3K4 trimethylation more frequently acquire active histone modifications during maturation. Taken together, these findings suggest that H3K4 trimethylation is required for the activation of genes involved in the functional maturation of pancreatic islet endocrine cells.

2021-05-21 | GSE174751 | GEO

Circulating lymphoid committed progenitors after allogeneic stem cell transplantation in humans

Project description:Lymphoid committed CD34+lin-CD10+CD24- progenitors undergo a rebound at month 3 after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in the absence of acute graft-versus-host disease (aGVHD). Here, we analyzed transcriptional programs of cell-sorted circulating lymphoid committed progenitors and CD34+Lin-CD10- non lymphoid progenitors in 11 allo-HSCT patients having (n=5) or not developed (n=6) grade 2 or 3 aGVHD and in 7 age-matched healthy donors. Major deregulated pathways included protein synthesis, energy production, cell cycle regulation and cytoskeleton organization. Notably, genes from protein biogenesis, translation machinery and cell cycle (CDK6) were over-expressed in progenitors from patients in the absence of aGVHD compared with healthy donors and patients affected by aGVHD. Expression of many genes from the mitochondrial oxidative phosphorylation metabolic pathway leading to ATP production were more specifically increased in lymphoid committed progenitors in absence of aGVHD. This was also the case for genes involved in cell mobilization such as those regulating Rho GTPases activity. In all, we show that circulating lymphoid committed progenitors undergo profound changes in metabolism favoring cell proliferation, energy production and cell mobilization after allo-HSCT in humans. These mechanisms are abolished in case of aGVHD or its treatment, indicating a persistent cell-intrinsic defect after exit from bone marrow.

2018-11-14 | GSE75344 | GEO

Open chromatin landscape of pancreatic endocrine progenitors

Project description:During embryonic development, islet progenitors are specified from pancreatic duct cells by transient expression of Neurog3, a transcription factor necessary and sufficient for initiation of islet development. To understand the dynamics of Neurog3-dependent endocrine cell fate determination, in this study we used ATAC-Seq to identify accessible genomic regions of purified duct, endocrine progenitor, and endocrine cells isolated from mice with varying Neurog3 dosage

2020-04-01 | GSE65794 | GEO

Comparison of endocrine enriched genes in islet beta cells versus induced beta cells

2008-07-08 | GSE12025 | GEO

Comparison of endocrine enriched genes in islet beta cells versus induced beta cells

Project description:Endocrine enriched genes in adult islet beta cells were identified and compared with that of induced beta cells (with M3 transcription factors) in adult. The control sample is non-beta pancreatic cells. Gene expression profile comparison of 3 samples, 3 independent repeats for each sample indicate a high degree of similarity between endogenous and induced beta cells in adult mouse.

2008-07-08 | E-GEOD-12025 | biostudies-arrayexpress

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