ArticleThe Journal of biological chemistry2014
Inhibition of pancreatic β-cell Ca2+/calmodulin-dependent protein kinase II reduces glucose-stimulated calcium influx and insulin secretion, impairing glucose tolerance.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
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- The role of mitochondrial-associated endoplasmic reticulum membranes (MAMs) in diabetic microvascular complications: a review.Cell death & disease · 2025Review
- Expanding the phenotype of CARS1 variants to include congenital hyperinsulinism.BMC medical genomics · 2025Article
- Enhanced dynorphin expression and secretion in pancreatic beta-cells under hyperglycemic conditions.Molecular metabolism · 2025Article
- A negative regulatory role of β-cell-derived exosomes in the glucose-stimulated insulin secretion of recipient β-cells.Archives of toxicology · 2024Article
- (+)-Catechin mitigates impairment in insulin secretion and beta cell damage in methylglyoxal-induced pancreatic beta cells.Molecular biology reports · 2024Article
- Molecular mechanism responsible for sex differences in electrical activity of mouse pancreatic β cells.JCI insight · 2024Article
- CaFrontiers in endocrinology · 2024Review
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- Context-dependent effects of CCN2 on β-cell mass expansion and indicators of cell stress in the setting of acute and chronic stress.American journal of physiology. Endocrinology and metabolism · 2023Article
- Article
- The functions of CaJournal of cell communication and signaling · 2023Review
- [Role of CaMK II in pancreatic injury in mice with severe acute pancreatitis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Pharmacological blockade of the EP3 prostaglandin EMolecular metabolism · 2021Article
- Heart failure in diabetes.Metabolism: clinical and experimental · 2021Review
- TRPM7 is a crucial regulator of pancreatic endocrine development and high-fat-diet-induced β-cell proliferation.Development (Cambridge, England) · 2021Article
- Key Metabolic Functions of β-Arrestins: Studies with Novel Mouse Models.Trends in endocrinology and metabolism: TEM · 2021Review
- Myt Transcription Factors Prevent Stress-Response Gene Overactivation to Enable Postnatal Pancreatic β Cell Proliferation, Function, and Survival.Developmental cell · 2020Article
- Primary cilia control glucose homeostasis via islet paracrine interactions.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Obesity-induced overexpression of miR-802 impairs insulin transcription and secretion.Nature communications · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells is caused by Ca(2+) entry via voltage-dependent Ca(2+) channels. CaMKII is a key mediator and feedback regulator of Ca(2+) signaling in many tissues, but its role in β-cells is poorly understood, especially in vivo. Here, we report that mice with conditional inhibition of CaMKII in β-cells show significantly impaired glucose tolerance due to decreased GSIS. Moreover, β-cell CaMKII inhibition dramatically exacerbates glucose intolerance following exposure to a high fat diet. The impairment of islet GSIS by β-cell CaMKII inhibition is not accompanied by changes in either glucose metabolism or the activities of KATP and voltage-gated potassium channels. However, glucose-stimulated Ca(2+) entry via voltage-dependent Ca(2+) channels is reduced in islet β-cells with CaMKII inhibition, as well as in primary wild-type β-cells treated with a peptide inhibitor of CaMKII. The levels of basal β-cell cytoplasmic Ca(2+) and of endoplasmic reticulum Ca(2+) stores are also decreased by CaMKII inhibition. In addition, CaMKII inhibition suppresses glucose-stimulated action potential firing frequency. These results reveal that CaMKII is a Ca(2+) sensor with a key role as a feed-forward stimulator of β-cell Ca(2+) signals that enhance GSIS under physiological and pathological conditions.
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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 Socratic graph.