ArticleArchives of biochemistry and biophysics2010
Lower succinyl-CoA:3-ketoacid-CoA transferase (SCOT) and ATP citrate lyase in pancreatic islets of a rat model of type 2 diabetes: knockdown of SCOT inhibits insulin release in rat insulinoma cells.
Article in Archives of biochemistry and biophysics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Identification of the regulatory elements and protein substrates of lysine acetoacetylation.eLife · 2026Article
- Succinylation modification in diabetes and diabetic complications: Mechanisms and functions (Review).Molecular medicine reports · 2026Review
- Review
- Identification of the Regulatory Elements and Protein Substrates of Lysine Acetoacetylation.bioRxiv : the preprint server for biology · 2025Article
- Succinylation enables IDE to act as a hub of larval tissue destruction and adult tissue reconstruction during insect metamorphosis.Science advances · 2025Article
- Metabolic cycles and signals for insulin secretion.Cell metabolism · 2022Review
- Redefining the coenzyme A transferase superfamily with a large set of manually annotated proteins.Protein science : a publication of the Protein Society · 2022Article
- Islet Health, Hormone Secretion, and Insulin Responsivity with Low-Carbohydrate Feeding in Diabetes.Metabolites · 2020Review
- The vital role of ATP citrate lyase in chronic diseases.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Factors Influencing Mitochondrial Function as a Key Mediator of Glucose-Induced Insulin Release: Highlighting Nicotinamide Nucleotide Transhydrogenase.International journal of molecular and cellular medicine · 2020Review
- Metabolic fate of glucose and candidate signaling and excess-fuel detoxification pathways in pancreatic β-cells.The Journal of biological chemistry · 2017Article
- Knockdown of ATP citrate lyase in pancreatic beta cells does not inhibit insulin secretion or glucose flux and implicates the acetoacetate pathway in insulin secretion.Molecular metabolism · 2016Article
- Characterization of phospholipids in insulin secretory granules and mitochondria in pancreatic beta cells and their changes with glucose stimulation.The Journal of biological chemistry · 2015Article
- Comparative Analysis of the Mitochondrial Physiology of Pancreatic β Cells.Bioenergetics : open access · 2014Article
- Ketone body metabolism and cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2013Review
- Metabolome response to glucose in the β-cell line INS-1 832/13.The Journal of biological chemistry · 2013Article
- Knockdown of pyruvate carboxylase or fatty acid synthase lowers numerous lipids and glucose-stimulated insulin release in insulinoma cells.Archives of biochemistry and biophysics · 2013Article
- Mitochondrial proteomic analysis reveals deficiencies in oxygen utilization in medullary thick ascending limb of Henle in the Dahl salt-sensitive rat.Physiological genomics · 2012Article
- A distinct metabolic signature predicts development of fasting plasma glucose.Journal of clinical bioinformatics · 2012Article
- Sphingosine kinase 1 knockdown reduces insulin synthesis and secretion in a rat insulinoma cell line.Archives of biochemistry and biophysics · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Succinyl-CoA:3-ketoacid-CoA transferase (SCOT) is a mitochondrial enzyme that catalyzes the reversible transfer of coenzyme-A from acetoacetyl-CoA to succinate to form acetoacetate and succinyl-CoA. mRNAs of SCOT and ATP citrate lyase were decreased 55% and 58% and enzyme activities were decreased >70% in pancreatic islets of the GK rat, a model of type 2 diabetes. INS-1 832/13 cells were transfected with shRNAs targeting SCOT mRNA to generate cell lines with reduced SCOT activity. Two cell lines with >70% knockdown of SCOT activity showed >70% reduction in glucose- or methyl succinate-plus-beta-hydroxybutyrate-stimulated insulin release. Less inhibition of insulin release was observed with two cell lines with less knockdown of SCOT. Previous studies showed knockdown of ATP citrate lyase in INS-1 832/13 cells does not lower insulin release. The results further support work that suggests mitochondrial pathways involving SCOT which supply acetoacetate for export to the cytosol are important for insulin secretion.
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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.