ArticleDiabetes2015
Novel stable isotope analyses demonstrate significant rates of glucose cycling in mouse pancreatic islets.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Distinct bile mycobiome signature identifies fungal peptide panel predictive for gallbladder carcinoma.Molecular therapy. Oncology · 2026Article
- G6PC2 controls glucagon secretion by defining the set point for glucose in pancreatic α cells.Science translational medicine · 2025Article
- Deciphering sphingolipid biosynthesis dynamics iniScience · 2024Article
- Biochemical and metabolic characterization of a G6PC2 inhibitor.Biochimie · 2024Article
- Identification of structural motifs critical for human G6PC2 function informed by sequence analysis and an AlphaFold2-predicted model.Bioscience reports · 2024Article
- Observing exocrine pancreas metabolism using a novel pancreas perfusion technique in combination with hyperpolarized [1-Magnetic resonance in chemistry : MRC · 2023Article
- G6PC1 and G6PC2 influence G6P flux but not HSD11B1 activity.Journal of molecular endocrinology · 2023Article
- Haplotypes of the genes (GCK and G6PC2) underlying the glucose/glucose-6-phosphate cycle are associated with pancreatic beta cell glucose sensitivity in patients with newly diagnosed type 2 diabetes from the VNDS study (VNDS 11).Journal of endocrinological investigation · 2021Article
- G6PC2 confers protection against hypoglycemia upon ketogenic diet feeding and prolonged fasting.Molecular metabolism · 2020Article
- Tracing metabolic flux through time and space with isotope labeling experiments.Current opinion in biotechnology · 2020Review
- Pancreatic islet beta cell-specific deletion of G6pc2 reduces fasting blood glucose.Journal of molecular endocrinology · 2020Article
- Integrated In Vivo Quantitative Proteomics and Nutrient Tracing Reveals Age-Related Metabolic Rewiring of Pancreatic β Cell Function.Cell reports · 2018Article
- Effects ofJournal of molecular endocrinology · 2017Article
- G6PC2 Modulates the Effects of Dexamethasone on Fasting Blood Glucose and Glucose Tolerance.Endocrinology · 2016Article
- G6PC2 Modulates Fasting Blood Glucose In Male Mice in Response to Stress.Endocrinology · 2016Article
- Article
- Article
- Mass spectrometry-based microassay of (2)H and (13)C plasma glucose labeling to quantify liver metabolic fluxes in vivo.American journal of physiology. Endocrinology and metabolism · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A polymorphism located in the G6PC2 gene, which encodes an islet-specific glucose-6-phosphatase catalytic subunit, is the most important common determinant of variations in fasting blood glucose (FBG) levels in humans. Studies of G6pc2 knockout (KO) mice suggest that G6pc2 represents a negative regulator of basal glucose-stimulated insulin secretion (GSIS) that acts by hydrolyzing glucose-6-phosphate (G6P), thereby reducing glycolytic flux. However, this conclusion conflicts with the very low estimates for the rate of glucose cycling in pancreatic islets, as assessed using radioisotopes. We have reassessed the rate of glucose cycling in pancreatic islets using a novel stable isotope method. The data show much higher levels of glucose cycling than previously reported. In 5 mmol/L glucose, islets from C57BL/6J chow-fed mice cycled ∼16% of net glucose uptake. The cycling rate was further increased at 11 mmol/L glucose. Similar cycling rates were observed using islets from high fat-fed mice. Importantly, glucose cycling was abolished in G6pc2 KO mouse islets, confirming that G6pc2 opposes the action of the glucose sensor glucokinase by hydrolyzing G6P. The demonstration of high rates of glucose cycling in pancreatic islets explains why G6pc2 deletion enhances GSIS and why variants in G6PC2 affect FBG in humans.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.