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Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

ABSTRACT: Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

PROVIDER: PRJNA761990 | ENA |

REPOSITORIES: ENA

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Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

Project description:Selenium is an essential trace element that has gained interest for its potential role in glucose homeostasis. The purpose of the present study was to investigate the impact of selenium supplementation as selenomethionine (SeMet) on insulin secretion in MIN6-K8 cells, a model of pancreatic -cells. We found that 40 μM and 80 μM SeMet significantly enhanced percent insulin secretion at low (2.8 mM), intermediate (11.7 mM), and high (16.7 mM) glucose stimulation. SeMet also increased tolbutamide- or KCl-induced percent insulin secretion at 40 μM and 80 μM. Ca2+ influx was only reduced with 80 μM SeMet. RNA-sequencing showed that 40 μM SeMet supplementation upregulated expression of selenoprotein H (SelH) and thioredoxin reductase 1 (Txnrd 1) and downregulated expression of glutathione peroxidase 3 (Gpx3), selenoprotein O (SelO), and selenoprotein P (SelP). Gpx3 knockdown increased both percent and total insulin release with high glucose stimulation. SelP knockdown increased insulin release at high glucose. In conclusion, high SeMet supplementation augments insulin secretion, while reductions in Gpx3 and SelP expression, from SeMet supplementation or via silencing, augment -cell function in the MIN6-K8 cell line. These studies support a putative role for selenium and selenoproteins in the regulation of glucose homeostasis and diabetes risk.

2024-03-13 | GSE183775 | GEO

Selenomethionine modulates insulin secretion in the MIN6-K8 mouse insulinoma cell line.

Project description:Selenium is an essential trace element of interest for its potential role in glucose homeostasis. The present study investigated the impact of selenium supplementation as selenomethionine (SeMet) on insulin secretion in MIN6-K8 cells, a pancreatic β-cell model. We found that SeMet enhanced percent glucose-induced insulin secretion, while also increasing tolbutamide- and KCl-induced percent insulin secretion. RNA-sequencing showed that SeMet supplementation altered expression of several selenoproteins, including glutathione peroxidase 3 (Gpx3) and selenoprotein P (SelP). Targeted knockdown of Gpx3 increased both percent and total insulin release, while SelP knockdown increased insulin content and insulin release. Collectively, these studies support a putative role for selenium and selenoproteins in the regulation of insulin secretion, glucose homeostasis, and diabetes risk.

| S-EPMC10924436 | biostudies-literature

Modulation of insulin secretion through RBFOX2-mediated alternative splicing [RNA-seq MIN6]

Project description:Recent studies have identified dysregulation of RNA-binding proteins (RBPs) and aberrant mRNA splicing in the onset of diseases including diabetes. Here we investigated the role of RBFOX2 in the pancreatic β cell through the conditional mutation of Rbfox2 in the mouse pancreas (Pdx1:Cre; Rbfox2fl/lf) and RNAi experiments in the mouse insulinoma cell line, MIN6. We then identified the direct targets of RBFOX2 in the mouse β cell transcriptome my eCLIP-Seq in MIN6 cells.

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Modulation of insulin secretion through RBFOX2-mediated alternative splicing [eCLIP-Seq MIN6]

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Transcription profiling of mouse MIN6 insulinoma beta cells following knock-down of murine Pdx1

Project description:In order to identify genes that are regulated by Pdx1, MIN6 insulinoma cells were transduced with adenovirus expressing a short hairpin RNA directed against murine Pdx1 (AdshPdx1) or luciferase (AdshLuc) or not transduced at all (untreated). RNA was harvested and reverse transcribed. Reduced expression of Pdx1 and established Pdx1 targets was confirmed. The RNA was then submitted for labeling and hybridization to the PancChip cDNA microarray.

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Sustained hyperglycemia specifically targets translation of mRNAs for insulin secretion

Project description:Pancreatic beta-cells are specialized for coupling glucose metabolism to insulin peptide production and secretion. Acute glucose exposure robustly and coordinately increases translation of proinsulin and proteins required for secretion of mature insulin peptide. By contrast, chronically elevated glucose levels that occur during diabetes impair beta-cell insulin secretion and have been shown experimentally to suppress insulin translation. Whether translation of other genes critical for insulin secretion are similarly downregulated by chronic high glucose is unknown. Here, we used high-throughput ribosome profiling and nascent proteomics in MIN6 insulinoma cells to elucidate the genome-wide impact of sustained high glucose on beta-cell mRNA translation. Prior to induction of ER stress or suppression of global translation, sustained high glucose suppressed glucose-stimulated insulin secretion and downregulated translation of not only insulin, but also of mRNAs related to insulin secretory granule formation, exocytosis, and metabolism-coupled insulin secretion. Translation of these mRNAs was also downregulated in primary rat and human islets following ex-vivo incubation with sustained high glucose and in an in vivo model of chronic mild hyperglycemia. Furthermore, translational downregulation decreased cellular abundance of these proteins. Our study uncovered a translational regulatory circuit during beta-cell glucose toxicity that impairs expression of proteins with critical roles in beta-cell function.

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Transcription profiling by array of mouse pancreatic beta cells of MIN6 insulinoma cell line transfected with siRNA directed against murine Meis3 or non targeting control.

Project description:In order to identify genes that are regulated by Meis3, MIN6 insulinoma cells were transfected with siRNA directed against murine Meis3 (siMeis3) or non targeting control (siControl). RNA was harvested and reverse transcribed. Reduced expression of Meis3 was confirmed. The RNA was then submitted for labeling and hybridization to the Agilent cDNA microarray.

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Modulation of insulin secretion through RBFOX2-mediated alternative splicing [RNA-seq MIN6]

Project description:Modulation of insulin secretion through RBFOX2-mediated alternative splicing [RNA-seq MIN6]

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Modulation of insulin secretion through RBFOX2-mediated alternative splicing [eCLIP-Seq MIN6]

Project description:Modulation of insulin secretion through RBFOX2-mediated alternative splicing [eCLIP-Seq MIN6]

| PRJNA913819 | ENA