Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
239
datasets available to search
ShareScore release 0.9.0
Dataset results
239 results for “β-Cell”
β-cell-specific deletion of Zfp148 improves nutrient-stimulated β-cell Ca2+ responses
<p>Insulin secretion from pancreatic β-cells is essential for glucose homeostasis. An insufficient response to the demand for insulin results in diabetes. We previously showed that β-cell-specific deletion of <em>Zfp148</em> (β-<em>Zfp148</em><sup>KO</sup>) improves glucose tolerance and insulin secretion in mice. Here, we performed Ca<sup>2+</sup> imaging of islets from β‑<em>Zfp148</em><sup>KO</sup> and control mice on both a chow and a Western-style diet. β-<em>Zfp148</em><sup>KO</sup> islets demonstrate improved sensitivity and sustained Ca<sup>2+</sup> oscillations in response to elevated glucose. β-<em>Zfp148</em><sup>KO</sup> islets also exhibit elevated sensitivity to amino acid-induced Ca<sup>2+</sup> influx under low glucose conditions, suggesting enhanced mitochondrial phosphoenolpyruvate (PEP)-dependent KATP channel closure, independent of glycolysis. RNA sequencing and proteomics of β-<em>Zfp148</em><sup>KO</sup> islets revealed altered levels of enzymes involved in amino acid metabolism (SLC3A2, SLC7A8, GLS, GLS2, PSPH, PHGDH, PSAT1) and intermediary metabolism (GOT1, PCK2), consistent with altered PEP cycling. In agreement with this, β-<em>Zfp148</em><sup>KO</sup> islets displayed enhanced insulin secretion in response to L-glutamine and activation of glutamate dehydrogenase. Understanding pathways controlled by ZFP148 may provide promising strategies for improving β-cell function that are robust to the metabolic challenge imposed by a Western diet.</p>
β-cell-specific deletion of Zfp148 improves nutrient-stimulated β-cell Ca2+ responses
Open the record for dataset details and reuse information.
Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling
<p class="MsoNormal"><span>Endogenous </span><span>humoral factors </span><span>that</span><span> link systemic and/or local insulin demand to pancreatic β-cells have not been identified. Here</span><span>,</span><span> we demonstrated that T-cadherin, a unique glycosylphosphatidylinositol-anchored cadherin primarily expressed in vascular endothelial cells and cardiac and skeletal muscle cells, but not in pancreatic β-cells, was secreted as soluble forms and was important for β-cell proliferation. <em>Cdh13</em> (T-cadherin) knockout mice exhibited impaired glucose handling due to attenuated β-cell proliferation under high-fat diet conditions. The gene expression analyses indicated the impairment in cell cycle and Notch signaling in the islets of T-cadherin knockout mice under high-fat diet conditions. In streptozotocin-induced diabetes, the replacement of soluble T-cadherin improved β-cell mass and blood glucose </span><span>levels</span><span> in T-cadherin knockout mice. </span><span>R</span><span>ecombinant soluble T-cadherin upregulated Notch signaling in cultured murine islets. We concluded that soluble T-cadherin could work as an endogenous humoral factor whose signaling pathways including Notch signaling regulate β-cell proliferation under diabetic conditions in mice.</span></p>
Small things matter: Lack of extra-islet β-cells in Type 1 diabetes
Open the record for dataset details and reuse information.
Data from: ApoA-I protects pancreatic β-cells from cholesterol-induced mitochondrial damage and restores their ability to secrete insulin
Open the record for dataset details and reuse information.
Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling
Open the record for dataset details and reuse information.
Effect of Microvesicles and Exosomes Therapy on β-cell Mass in Type I Diabetes Mellitus (T1DM)
ClinicalTrials.gov study NCT02138331. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Dietary Oxysterols and β-Cell Function Among African Americans
ClinicalTrials.gov study NCT05072587. IPD Sharing: NO. Countries: 1. Publications: 39.
The Acute Effects of Low-dose TNF-α on Glucose Metabolism and β-cell Function in Humans
ClinicalTrials.gov study NCT01953393. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Probiotic Supplementation and Pancreatic β-Cell Function in Type 2 Diabetes
ClinicalTrials.gov study NCT05765292. IPD Sharing: NO. Countries: 1. Publications: 1.
Diet Composition and Physical Inactivity on Insulin Sensitivity and β-cell Function
ClinicalTrials.gov study NCT03013764. IPD Sharing: NO. Countries: 1. Publications: 1.
Clinical Trial to Assess the Effects of Dairy on Insulin Sensitivity and β-Cell Function
ClinicalTrials.gov study NCT01936935. IPD Sharing: Not stated. Countries: 1. Publications: 1.
LncRNA-Malat1 is involved in lipotoxicity-induced β-cell dysfunction and the therapeutic effect of exendin-4 via Ptbp1
Open the record for dataset details and reuse information.
Code from: PID-controller enhanced artificial β-cells
Open the record for dataset details and reuse information.
Data from: Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells
ATP-sensitive potassium channels (KATP channels) are critical nutrient sensors in many mammalian tissues. In the pancreas, KATP channels are essential for coupling glucose metabolism to insulin secretion. While orthologous genes for many components of metabolism–secretion coupling in mammals are present in lower vertebrates, their expression, functionality and ultimate impact on body glucose homeostasis are unclear. In this paper, we demonstrate that zebrafish islet β-cells express functional KATP channels of similar subunit composition, structure and metabolic sensitivity to their mammalian counterparts. We further show that pharmacological activation of native zebrafish KATP using diazoxide, a specific KATP channel opener, is sufficient to disturb glucose tolerance in adult zebrafish. That β-cell KATP channel expression and function are conserved between zebrafish and mammals illustrates the evolutionary conservation of islet metabolic sensing from fish to humans, and lends relevance to the use of zebrafish to model islet glucose sensing and diseases of membrane excitability such as neonatal diabetes.
Data from: An increase in immature β-cells lacking Glut2 precedes the expansion of β-cell mass in the pregnant mouse
A compensatory increase in β-cell mass occurs during pregnancy to counter the associated insulin resistance, and a failure in adaptation is thought to contribute to gestational diabetes. Insulin-expressing but glucose-transporter-2-low (Ins+Glut2LO) progenitor cells are present in mouse and human pancreas, being predominantly located in extra-islet β-cell clusters, and contribute to the regeneration of the endocrine pancreas following induced ablation. We therefore sought to investigate the contribution of Ins+Glut2LO cells to β-cell mass expansion during pregnancy. Female C57Bl/6 mice were time mated and pancreata were collected at gestational days (GD) 6, 9, 12, 15, and 18, and postpartum D7 (n = 4/time-point) and compared to control (non-pregnant) animals. Beta cell mass, location, proliferation (Ki67+), and proportion of Ins+Glut2LO cells were measured using immunohistochemistry and bright field or confocal microscopy. Beta cell mass tripled by GD18 and β-cell proliferation peaked at GD12 in islets (≥6 β-cells) and small β-cell clusters (1–5 β-cells). The proportion and fraction of Ins+Glut2LO cells undergoing proliferation increased significantly at GD9 in both islets and clusters, preceding the increase in β-cell mass and proliferation, and their proliferation within clusters persisted until GD15. The overall number of clusters increased significantly at GD9. Quantitative PCR showed a significant increase in Pdx1 presence at GD9 vs. GD18 or control pancreas, and Pdx1 was visualized by immunohistochemistry within both Ins+Glut2LO and Ins+Glut2HI cells within clusters. These results indicate that Ins+Glut2LO cells are likely to contribute to β-cell mass expansion during pregnancy.
Raw Data for the article: In Vitro Evaluation of Nanoerythrosome Cytotoxicity and Uptake in Pancreatic Endothelial Cells: Implications for β-Cell Imaging Applications
<p>Biomolecule-targeted imaging represents one of the most difficult challenges in medicine. Nanoerythrosomes (NERs) are nanovesicles obtained after lysis of red blood cells, and they are promising tools for drug delivery and imaging. In this work, a formulation based on NERs functionalized with 7-amino-3-methylcoumarin via cross-linking was tested on rat INS-1E and mouse MIN6 β-cells and endothelial MSI cell lines. First, the morphology, size, ζ-potentials, and spectroscopic properties of the aggregates were investigated, highlighting that the functionalization did not significantly affect the nanoparticles' physicochemical features. <em>In vitro</em>, the nanoparticles did not significantly affect the proliferation and function of INS-1E and MIN6 β-cells at different concentrations. Only at the highest concentration tested on the MSI cell line, the formulation inhibited proliferation. Furthermore, NER aggregates were not internalized in both INS-1E and MIN6 cell lines, while a diffuse fluorescence was noticed in the cytosol of the MSI cell line at the highest concentrations. These findings proved that NER formulations might represent a new nanotool for β-cell imaging as a part of a strategy aimed to prevent any intracellular accumulation, thus reducing/avoiding side effects.</p>
Effect of Intensive Therapy Associated With CSII on β-cell Function With Newly Diagnosed Type 2 Diabetes
ClinicalTrials.gov study NCT00948324. IPD Sharing: Not stated. Countries: 0. Publications: 1.
Urine Extracellular Vesicles: Non-invasive Biomarkers of Β-cell Function and Novel Therapeutic Agents in Diabetes
ClinicalTrials.gov study NCT06832215. IPD Sharing: NO. Countries: 1. Publications: 0.
Effects of Different Early Intensive Therapies on Long-term β-cell Function
ClinicalTrials.gov study NCT01471808. IPD Sharing: NO. Countries: 0. Publications: 1.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.