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3,861 results for “Glucose”
Single-cell transcriptomic profiling of human pancreatic islets reveals genes responsive to glucose exposure over 24 hours
<p><strong>Aims/hypothesis</strong>: Disruption of pancreatic islet function and glucose homeostasis can lead to the development of sustained hyperglycemia, beta cell glucotoxicity, and subsequently type 2 diabetes. In this study, we explored the effects of <em>in vitro</em> hyperglycemic conditions on human pancreatic islet gene expression across 24 hours in six pancreatic cell types: alpha, beta, gamma, delta, ductal, and acinar cells. We hypothesized that genes associated with hyperglycemic conditions may be relevant to the onset and progression of diabetes.</p> <p><strong>Methods</strong>: We exposed human pancreatic islets from two donors to low (2.8 mmol/l) and high (15.0 mmol/l) glucose concentrations over 24 hours <em>in vitro</em>. To assess the transcriptome, we performed single-cell RNA sequencing (scRNA-seq) at seven time points. We modeled time as both a discrete and continuous variable to determine momentary and longitudinal changes in transcription associated with islet time in culture or glucose exposure. Additionally, we integrated genomic features and genetic summary statistics to nominate candidate effector genes. For three of these genes, we functionally characterized the effect on insulin production and secretion using CRISPR interference to knockdown gene expression in EndoC-βH1 cells, followed by a glucose-stimulated insulin secretion assay.</p> <p><strong>Results</strong>: Across all cell types, we identified 1,447 genes associated with time, 680 genes associated with glucose exposure, and 418 genes associated with interaction effects between time and glucose. By integrating these expression profiles with summary statistics from genetic association studies, we identified 2,449 candidate effector genes for type 2 diabetes, HbA1c, random blood glucose, and fasting blood glucose. Of these candidate effector genes, we showed that three—<em>ERO1B</em>, <em>HNRNPA2B1</em>, and <em>RHOBTB3</em>—exhibited an effect on glucose-stimulated insulin secretion and production in EndoC-βH1 cells.</p> <p><strong>Conclusions/interpretation</strong>: The findings of our study provide an in-depth characterization of the 24-hour transcriptomic response of human pancreatic islets to glucose exposure at a single-cell resolution. By integrating differentially expressed genes with genetic signals for type 2 diabetes and glucose-related traits, we provide insights into the molecular mechanisms underlying glucose homeostasis. Finally, we provide functional evidence to support the role of three candidate effector genes in insulin secretion and production.</p>
Data from: Trophic guilds differ in blood glucose concentrations: A phylogenetic comparative analysis in birds
<p>Glucose is a central metabolic compound used as a source of energy across all animal taxa. There is high interspecific variation in glucose concentration between taxa, the origin and the consequence of which remain largely unknown. Nutrition may affect glucose concentrations because carbohydrate content of different food sources may determine the importance of metabolic pathways in the organism. Birds sustain high glucose concentrations that may entail the risks of oxidative damage. We collected glucose concentration and life history data from 202 bird species from 171 scientific publications; classified them into seven trophic guilds and analysed the data with a phylogenetically controlled model. We show that glucose concentration is negatively associated with body weight and is significantly associated with trophic guilds with a moderate phylogenetic signal. After controlling for allometry, glucose concentrations were highest in carnivorous birds, which rely on high rates of gluconeogenesis to maintain their glycemia and lowest in frugivorous/nectarivorous species, which intake carbohydrates directly. However, trophic guilds with different glucose concentrations did not differ in lifespan. These results link nutritional ecology to physiology and suggest that at the macroevolutionary scale, species requiring constantly elevated glucose concentrations may have additional adaptations to avoid the risks associated with high glycemia.</p>
Raw data for the paper entitled "Astrocytic GLUT1 Reduction Paradoxically Improves Central and Peripheral Glucose Homeostasis"
<p>This files contains the raw data for all the figures contained in the paper entitled "Astrocytic GLUT1 Reduction Paradoxically Improves Central and Peripheral Glucose Homeostasis".</p>
GCK variants and their annotations for "Underestimated risk of secondary complications in pathogenic and glucose-elevating GCK variant carriers with type 2 diabetes"
<p>This file provides annoatations for GCK variants as dsecribed in "Underestimated risk of secondary complications in pathogenic and glucose-elevating GCK variant carriers with type 2 diabetes"</p>
Raman Datasets gathered from pure glucose liquid with 10 molar concentration
<p><span>With the purpose of replicating blood samples with a determined glucose level in our laboratory, we created samples by combining pure glucose and deionized water in a particular ratio. Main components used for measurements consist of:</span></p> <p><span><span>●<span> </span></span></span><span>Raman spectrophotometer: uRaman - Ci, Technospex.</span></p> <p><span><span>●<span> </span></span></span><span>Glucose chemical products: 99.5% Sigma-Aldrich glucose.</span></p> <p><span><span>●<span> </span></span></span><span>Deionized water solution bottle.</span></p> <p><span><span>●<span> </span></span></span><span>Tools<span> </span>(solution tube, stirring rod,…).</span></p> <p><span>The measurement procedure is described as below:</span></p> <p><span><span>1.<span> </span></span></span><span>Set excitation laser power to 100mW.</span></p> <p><span><span>2.<span> </span></span></span><span>Set the measurement range at the wavelength of 785.1nm in 300s.</span></p> <p><span><span>3.<span> </span></span></span><span>Place 3 ml of glucose solution from each of the mentioned test tubes on the quartz surface of the Cuvette.</span></p> <p><span><span>4.<span> </span></span></span><span>Insert the cuvette (with the MACRO-CH/Quartz Cuvette accessory) into the measurement chamber of the uRaman – Ci spectrophotometer.</span></p> <p><span><span>5.<span> </span></span></span><span>Collect digitized Raman signals from the measurement experiment.</span></p> <p> </p> <p> </p> <p> </p> <div> <table> <tbody> <tr> <td> <p><span>Glucose concentration level (mmol/L)</span></p> </td> <td> <p><span>Number of samples</span></p> </td> </tr> <tr> <td> <p><span>5.0</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>5.5</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>6.0</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>6.5</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>7.0</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>7.5</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>10.0</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>12.5</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>15.0</span></p> </td> <td> <p><span>5</span></p> </td> </tr> <tr> <td> <p><span>20.0</span></p> </td> <td> <p><span>5</span></p> </td> </tr> </tbody> </table> <p> </p> </div> <p> </p>
Electrochemically produced peroxydicarbonate for efficient gold catalysed oxidation of glucose to gluconic acid - Dataset
<p>Experimental data for glucose oxidation applying supported gold catalysts and peroxo-dicarbonate in comparison to other oxidants.</p>
Glycerol suppresses glucose consumption in trypanosomes through metabolic contest
<p>The file contains all the source data presented in the manuscript:</p> <p>Allmann S., M. Wargnies, E. Cahoreau, M. Biran, N. Plazolles, P. Morand, E. Pineda, H. Kulyk-Babier, C. Asencio, O. Villafraz, L. Rivière, E. Tetaud, B. Rotureau, A. Mourier, J.-C. Portais, & F. Bringaud (<strong>2021</strong>) Glycerol suppresses glucose consumption in Trypanosomes through metabolic contest. <strong><em>PLoS</em></strong> <strong><em>Biol</em></strong>.</p>
GTTAtlas - Metabolomics atlas of oral 13C-glucose tolerance test in mice
<p>GTTAtlas - Metabolomics atlas of oral <sup>13</sup>C<sub>6</sub>-glucose tolerance test in mice</p> <p>GTTAtlas web application: <a href="https://gttatlas.metabolomics.fgu.cas.cz">https://gttatlas.metabolomics.fgu.cas.cz</a></p> <p>Repository of LC–MS data in *.abf format: <a href="https://repository.metabolomics.fgu.cas.cz/">https://repository.metabolomics.fgu.cas.cz/</a></p> <p>LC–MS platforms: <a href="https://www.metabolomics.fgu.cas.cz">https://www.metabolomics.fgu.cas.cz</a></p> <p>LIMeX platforms: BEH Amide positive, BEH amide negative, HSS T3 negative, BEH C18 positive, BEH C18 positive-TG, BEH C18 negative</p> <p>LC−MS system: Vanquish UHPLC System (Thermo Fisher Scientific, Bremen, Germany) coupled to a Q Exactive Plus mass spectrometer (Thermo Fisher Scientific)</p> <p>Samples: plasma, liver, pancreas, kidney, heart, gastrocnemius muscle, soleus muscle, duodenum, jejunum, ileum, subcutaneous adipose tissue, epididymal adipose tissue, brown adipose tissue.</p> <p>Time points: 0, 15, 30, 60, 120, 180, 240 minutes</p>
Blood glucose modulation and safety of efferent vagus nerve stimulation in a type 2 diabetic rat model
<p class="MsoNormal"><span>Vagus nerve stimulation is emerging as a promising treatment for type 2 diabetes. Here, we evaluated the ability of stimulation of the vagus nerve to reduce glycaemia in awake, freely moving metabolically compromised rats. A model of type 2 diabetes (n=10) was induced using a high-fat diet and low doses of streptozotocin. Stimulation of the abdominal vagus nerve was achieved by pairing 15 Hz pulses on a distal pair of electrodes </span><span>with high-frequency blocking stimulation (26 kHz, 4 mA) on a proximal pair of electrodes to preferentially produce efferent conducting activity </span><span>(eVNS)</span><span>. </span><span>Stimulation was well tolerated in awake, freely moving rats. During 1 hour of eVNS, glycaemia decreased in 90% of subjects (-1.25±1.25 mM·h, <em>P</em>=0.017), and 2 dB above neural threshold was established as the most effective 'dose' of eVNS (<em>P</em>=0.009). Following 5 weeks of implantation, eVNS was still effective, resulting in significantly decreased glycaemia (-1.7±0.6 mM·h, <em>P</em>=0.003) during 1 hour of eVNS. There were no overt changes in fascicle area or signs of histopathological damage observed in implanted vagal nerve tissue following chronic implantation and stimulation. </span><span>Demonstration of the biocompatability and safety of eVNS in awake, </span><span>metabolically compromised</span><span> animals is a critical first step to establishing this therapy for clinical use. With further development, </span><span>eVNS could be a promising novel therapy for treating type 2 diabetes.</span></p>
Identification of glucose-6 phosphate dehydrogenase deficient patients by ATR-FTIR spectroscopy using partial least squares discriminant analysis in aqueous blood samples
<p>Dataset of associated MIR spectra collected in the titled study</p> <p>Baseline: spectrum of air</p> <p>Water: spectrum of deionised water</p> <p>P#_M/F_GD/P/C/T/U_WB/PL/RBC_D/AQ_R: sample spectrum with each section representing the following</p> <ul> <li>P#: patient number 1-30</li> <li>M (male) or F(Female)</li> <li>GD (G6PD deficient), P (Partially G6PD deficient), C & T & ET(Control), U(Unknown) <ul> <li>P10, P28, P29, & P30 were determined later to be P, C, C, P respectively</li> </ul> </li> <li>WB (whole blood), PL (plasma), RBC (red blood cells)</li> <li>D (dried sample spectrum), AQ (aqueous sample spectrum)</li> </ul>
Sirtuin3 ensures the metabolic plasticity of neurotransmission during glucose deprivation
<p>Neurotransmission is an energetically expensive process that underlies cognition. During intense electrical activity or dietary restrictions, glucose levels in the brain plummet, forcing neurons to utilize alternative fuels. However, the molecular mechanisms of neuronal metabolic plasticity remain poorly understood. Here, we demonstrate that glucose-deprived neurons activate the CREB and PGC1α transcriptional program that induces the expression of the mitochondrial deacetylase Sirtuin 3 (Sirt3) both <em>in vitro</em> and i<em>n vivo</em>. We show that Sirt3 localizes to axonal mitochondria and stimulates mitochondrial oxidative capacity in hippocampal nerve terminals. Sirt3 plays an essential role in sustaining synaptic transmission in the absence of glucose by powering the retrieval of synaptic vesicles after release. These results demonstrate that the transcriptional induction of Sirt3 ensures the metabolic plasticity of synaptic transmission.</p>
Chronic hyperadiponectinemia induced by transgenic overexpression increases plasma exosomes without significantly improving glucose and lipid metabolism
<p><span>The fat</span><span>-derived factor, adiponectin, is considered a salutary circulating factor.</span> <span>We recently demonstrated that native adiponectin binds T-cadherin and promotes intracellular biogenesis and secretion of the exosome. Exosomes play important roles in various aspects of homeostasis, including glucose and energy metabolism. However, it remains unclear whether and how the promotion of exosome production by adiponectin <em>in vivo</em> is beneficial for glucose and lipid metabolism. In the present study, overexpression of human adiponectin in mice resulted in an increased number of circulating exosomes, but it did not significantly improve glucose metabolism, change body weights, or change triglyceride clearance under a high-fat diet. Multiple small doses of streptozotocin increased blood glucose and decreased triglyceride clearance similarly in both wild-type and transgenic mice. Thus, these results indicated that human adiponectin overexpression in mice increases plasma exosomes but does not significantly influence glucose and lipid metabolism.</span></p>
In fission yeast, 65 non-essential mitochondrial proteins related to respiration and stress become essential in low-glucose conditions
<p><span>Mitochondria perform critical functions, including respiration, ATP production, small molecule metabolism, anti-oxidation, and they are involved in a number of human diseases. While the mitochondrial genome contains a small number of protein-coding genes, the vast majority of mitochondrial proteins are encoded by nuclear genes. In fission yeast, <em>Schizosaccharomyces</em> <em>pombe</em>, we screened 457 deletion (<em>del</em>) mutants deficient in nuclear-encoded mitochondrial proteins, searching for those that fail to form colonies in culture medium containing low glucose (0.03–0.1%; low-glucose sensitive, <em>lgs</em>), but that proliferate in regular 2–3% glucose medium. Sixty-five (14%) of the 457 deletion mutants displayed the <em>lgs</em> phenotype. Thirty-three of them are defective either in dehydrogenases, subunits of respiratory complexes, the TCA cycle, or in one of the 9 steps of the CoQ10 biosynthetic pathway. The remaining 32 <em>lgs</em> mutants do not seem to be directly related to respiration. Fifteen are implicated in translation, and 6 encode transporters. The remaining 11 function in anti-oxidation, amino acid synthesis, repair of DNA damage, microtubule cytoskeleton, intracellular mitochondrial distribution, or unknown functions. These 32 diverse <em>lgs</em> genes collectively maintain mitochondrial functions under low (1/20~1/60x normal) glucose concentrations. Interestingly, 30 of </span><span>them have homologs associated with human diseases. </span></p>
Low-glucose eating pattern and glycemic variability in women without diabetes who are at risk for postmenopausal breast cancer
<p>This dataset contains data collected and analysed for the paper, "<strong>A low-glucose eating pattern improves glycemic variability in women without diabetes who are at risk for postmenopausal breast cancer: An exploratory analysis of an RCT"</strong></p>
Aldosterone and Glucose Homeostasis
ClinicalTrials.gov study NCT00732160. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Closed Loop Glucose Control in Patients With Type 1 and Type 2 Diabetes
ClinicalTrials.gov study NCT05644730. IPD Sharing: NO. Countries: 1. Publications: 5.
Effect of Two Different Fasting Blood Glucose Targets on Glucose Control in Patients With Type 2 Diabetes Using Insulin Detemir Once Daily
ClinicalTrials.gov study NCT00634842. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Accuracy of the Dexcom G6 Continuous Glucose Monitoring System Following Cardiac Surgery
ClinicalTrials.gov study NCT04569240. IPD Sharing: NO. Countries: 1. Publications: 5.
An Exploratory Study of the Effects of Trelagliptin and Alogliptin on Glucose Variability in Patients With Type 2 Diabetes Mellitus
ClinicalTrials.gov study NCT02771093. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Feasibility and Clinical Utility of the Dexcom G6 Continuous Glucose Monitoring Device for Type 2 Diabetes
ClinicalTrials.gov study NCT05523362. IPD Sharing: NO. Countries: 1. Publications: 0.
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