ArticleDiabetes2016
Disallowance of Acot7 in β-Cells Is Required for Normal Glucose Tolerance and Insulin Secretion.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 33 citations in OpenAlex.
- In vivo functional profiling and structural characterization of the humanScience advances · 2026Article
- High-Protein Diet Exacerbates Insulin Resistance via the JNK/IKKβ-IRS-1 Pathway.Endocrinology, diabetes & metabolism · 2026Article
- Independent validation of lung adenocarcinoma prognostic risk scores incorporating cholesterol and estrogen metabolism related transcriptional biomarkers.Scientific reports · 2025Article
- Loss of β-cell identity and dedifferentiation, not an irreversible process?Frontiers in endocrinology · 2024Review
- Variable bioenergetic sensitivity of neurons and astrocytes to insulin and extracellular glucose.npj metabolic health and disease · 2024Article
- Metabolic cycles and signals for insulin secretion.Cell metabolism · 2022Review
- Differential regulation of mRNAs and lncRNAs related to lipid metabolism in Duolang and Small Tail Han sheep.Scientific reports · 2022Article
- Article
- A set of gene knockouts as a resource for global lipidomic changes.Scientific reports · 2022Article
- Acyl-CoA Thioesterase 7 is Transcriptionally Activated by Krüppel-Like Factor 13 and Promotes the Progression of Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021Article
- Metabolic and functional specialisations of the pancreatic beta cell: gene disallowance, mitochondrial metabolism and intercellular connectivity.Diabetologia · 2020Review
- Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation.Communications biology · 2020Article
- Review
- Cisplatin treatment of testicular cancer patients introduces long-term changes in the epigenome.Clinical epigenetics · 2019Article
- mTORC1 to AMPK switching underlies β-cell metabolic plasticity during maturation and diabetes.The Journal of clinical investigation · 2019Article
- The Impact of Pancreatic Beta Cell Heterogeneity on Type 1 Diabetes Pathogenesis.Current diabetes reports · 2018Review
- Cadmium-Associated Differential Methylation throughout the Placental Genome: Epigenome-Wide Association Study of Two U.S. Birth Cohorts.Environmental health perspectives · 2018Article
- Deactivating Fatty Acids: Acyl-CoA Thioesterase-Mediated Control of Lipid Metabolism.Trends in endocrinology and metabolism: TEM · 2017Review
- Raptor regulates functional maturation of murine beta cells.Nature communications · 2017Article
- Inflammatory stimuli induce acyl-CoA thioesterase 7 and remodeling of phospholipids containing unsaturated long (≥C20)-acyl chains in macrophages.Journal of lipid research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Encoding acyl-CoA thioesterase-7 (Acot7) is one of ∼60 genes expressed ubiquitously across tissues but relatively silenced, or disallowed, in pancreatic β-cells. The capacity of ACOT7 to hydrolyze long-chain acyl-CoA esters suggests potential roles in β-oxidation, lipid biosynthesis, signal transduction, or insulin exocytosis. We explored the physiological relevance of β-cell-specific Acot7 silencing by re-expressing ACOT7 in these cells. ACOT7 overexpression in clonal MIN6 and INS1(832/13) β-cells impaired insulin secretion in response to glucose plus fatty acids. Furthermore, in a panel of transgenic mouse lines, we demonstrate that overexpression of mitochondrial ACOT7 selectively in the adult β-cell reduces glucose tolerance dose dependently and impairs glucose-stimulated insulin secretion. By contrast, depolarization-induced secretion was unaffected, arguing against a direct action on the exocytotic machinery. Acyl-CoA levels, ATP/ADP increases, membrane depolarization, and Ca(2+) fluxes were all markedly reduced in transgenic mouse islets, whereas glucose-induced oxygen consumption was unchanged. Although glucose-induced increases in ATP/ADP ratio were similarly lowered after ACOT7 overexpression in INS1(832/13) cells, changes in mitochondrial membrane potential were unaffected, consistent with an action of Acot7 to increase cellular ATP consumption. Because Acot7 mRNA levels are increased in human islets in type 2 diabetes, inhibition of the enzyme might provide a novel therapeutic strategy.
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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.