ArticleDiabetes2013
G6PC2: a negative regulator of basal glucose-stimulated insulin secretion.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 4 of them syntheses that pooled it.
What it found
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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
49 citing papers in PubMed, 4 syntheses or guidelines pooled it, 86 citations in OpenAlex.
- Multi-omics analysis identifies CpGs near G6PC2 mediating the effects of genetic variants on fasting glucose.Diabetologia · 2021Pooled it
- Shared genetic architecture and casual relationship between leptin levels and type 2 diabetes: large-scale cross-trait meta-analysis and Mendelian randomization analysis.BMJ open diabetes research & care · 2020Pooled it
- Meta-analyses of the association of G6PC2 allele variants with elevated fasting glucose and type 2 diabetes.PloS one · 2017Pooled it
- Identification and functional characterization of G6PC2 coding variants influencing glycemic traits define an effector transcript at the G6PC2-ABCB11 locus.PLoS genetics · 2015Pooled it
- Prognostic model construction and drug prediction in colorectal cancer using mitochondrial programmed cell death-related genes.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Modelling the effects of human SUR1 R1420H variation on insulin secretory function using isogenic iPSC-derived pancreatic islets.Diabetologia · 2026Article
- From Human to Mouse and Back Again: Genetic and Genomic Ta(i)les of Islet Dysfunction in Type 2 Diabetes.Annual review of genetics · 2025Review
- Chicoric Acid and Chlorogenic Acid: Two Hydroxycinnamic Acids Modulate the Glucose 6-Phosphatase Activities in Pancreatic INS1 Beta-Cells-Novel Data in Favor of Two Putative Conformations of the G6Pase Within the ER Membrane.Molecules (Basel, Switzerland) · 2025Article
- Improving cellular fitness of human stem cell-derived islets under hypoxia.Nature communications · 2025Article
- HKDC1 promotes ovarian cancer progression through boosting lipid metabolism and immune escape by stabilizing G6PC/G6PC2.Communications biology · 2025Article
- Structural insights into glucose-6-phosphate recognition and hydrolysis by human G6PC1.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- G6PC2 controls glucagon secretion by defining the set point for glucose in pancreatic α cells.Science translational medicine · 2025Article
- Correlation of periodontitis with hepatic and intestinal inflammation and glycemic control, and effects of bioconvertedJournal of oral microbiology · 2025Article
- Multiple promoter and enhancer differences likely contribute to augmented G6PC2 expression in human versus mouse pancreatic islet alpha cells.Journal of molecular endocrinology · 2024Article
- The metabolic consequences of 'yo-yo' dieting are markedly influenced by genetic diversity.International journal of obesity (2005) · 2024Article
- Shared genetic architecture between periodontal disease and type 2 diabetes: a large scale genome-wide cross-trait analysis.Endocrine · 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
- Article
- G6PC1 and G6PC2 influence G6P flux but not HSD11B1 activity.Journal of molecular endocrinology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Elevated fasting blood glucose (FBG) is associated with increased risk for the development of type 2 diabetes and cardiovascular-associated mortality. Genome-wide association studies (GWAS) have linked polymorphisms in G6PC2 with variations in FBG and body fat, although not insulin sensitivity or glucose tolerance. G6PC2 encodes an islet-specific, endoplasmic reticulum-resident glucose-6-phosphatase catalytic subunit. A combination of in situ perfused pancreas, in vitro isolated islet, and in vivo analyses were used to explore the function of G6pc2 in mice. G6pc2 deletion had little effect on insulin sensitivity and glucose tolerance, whereas body fat was reduced in female G6pc2 knockout (KO) mice on both a chow and high-fat diet, observations that are all consistent with human GWAS data. G6pc2 deletion resulted in a leftward shift in the dose-response curve for glucose-stimulated insulin secretion (GSIS). As a consequence, under fasting conditions in which plasma insulin levels were identical, blood glucose levels were reduced in G6pc2 KO mice, again consistent with human GWAS data. Glucose-6-phosphatase activity was reduced, whereas basal cytoplasmic calcium levels were elevated in islets isolated from G6pc2 KO mice. These data suggest that G6pc2 represents a novel, negative regulator of basal GSIS that acts by hydrolyzing glucose-6-phosphate, thereby reducing glycolytic flux.
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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.