ArticleThe Journal of biological chemistry2014
Insulin protects pancreatic acinar cells from palmitoleic acid-induced cellular injury.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 53 citations in OpenAlex.
- Hypertriglyceridaemia-Associated Acute Pancreatitis: Pathophysiological Insights and Advances in Clinical Management.Biomedicines · 2026Review
- Breaking the Calcium Overload Cycle in Acute Pancreatitis: Emerging Pharmacological Strategies.Digestive diseases and sciences · 2026Review
- Combination of the CRAC Channel Inhibitor CM4620 and Galactose as a Potential Therapy for Acute Pancreatitis.Function (Oxford, England) · 2024Article
- The role of high serum triglyceride levels on pancreatic necrosis development and related complications.BMC gastroenterology · 2023Article
- Macronutrient Proportions and Fat Type Impact Ketogenicity and Shape the Circulating Lipidome in Dogs.Metabolites · 2022Article
- Stress Hyperglycemia Is Independently Associated with Persistent Organ Failure in Acute Pancreatitis.Digestive diseases and sciences · 2022Article
- The Prevalence and Characteristics of Exocrine Pancreatic Insufficiency in Patients with Type 2 Diabetes: A Systematic Review and Meta-Analysis.International journal of endocrinology · 2022Review
- Insulin protects acinar cells during pancreatitis by preserving glycolytic ATP supply to calcium pumps.Nature communications · 2021Article
- Donor insulin therapy in intensive care predicts early outcomes after pancreas transplantation.Diabetologia · 2021Article
- Dysregulated SREBP1c/miR-153 signaling induced by hypertriglyceridemia worsens acute pancreatitis and delays tissue repair.JCI insight · 2021Article
- Review
- Metabolic regulation of calcium pumps in pancreatic cancer: role of phosphofructokinase-fructose-bisphosphatase-3 (PFKFB3).Cancer & metabolism · 2020Article
- The Two-Way Relationship Between Calcium and Metabolism in Cancer.Frontiers in cell and developmental biology · 2020Review
- HOMA-estimated insulin resistance as an independent prognostic factor in patients with acute pancreatitis.Scientific reports · 2019Article
- Multimodal Transgastric Local Pancreatic Hypothermia Reduces Severity of Acute Pancreatitis in Rats and Increases Survival.Gastroenterology · 2019Article
- Galactose protects against cell damage in mouse models of acute pancreatitis.The Journal of clinical investigation · 2018Article
- Calcium signalling in the acinar environment of the exocrine pancreas: physiology and pathophysiology.The Journal of physiology · 2018Article
- Prediabetes Directly Deteriorates into Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Triggered by Acute Pancreatitis: A Case Report Illustrating a "Chicken and Egg" Paradigm in Ketosis-Prone Diabetes.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2018Article
- Metabolic regulation of the PMCA: Role in cell death and survival.Cell calcium · 2018Review
- The serum protein renalase reduces injury in experimental pancreatitis.The Journal of biological chemistry · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Acute pancreatitis is a serious and sometimes fatal inflammatory disease where the pancreas digests itself. The non-oxidative ethanol metabolites palmitoleic acid (POA) and POA-ethylester (POAEE) are reported to induce pancreatitis caused by impaired mitochondrial metabolism, cytosolic Ca(2+) ([Ca(2+)]i) overload and necrosis of pancreatic acinar cells. Metabolism and [Ca(2+)]i are linked critically by the ATP-driven plasma membrane Ca(2+)-ATPase (PMCA) important for maintaining low resting [Ca(2+)]i. The aim of the current study was to test the protective effects of insulin on cellular injury induced by the pancreatitis-inducing agents, ethanol, POA, and POAEE. Rat pancreatic acinar cells were isolated by collagenase digestion and [Ca(2+)]i was measured by fura-2 imaging. An in situ [Ca(2+)]i clearance assay was used to assess PMCA activity. Magnesium green (MgGreen) and a luciferase-based ATP kit were used to assess cellular ATP depletion. Ethanol (100 mM) and POAEE (100 μM) induced a small but irreversible Ca(2+) overload response but had no significant effect on PMCA activity. POA (50-100 μM) induced a robust Ca(2+) overload, ATP depletion, inhibited PMCA activity, and consequently induced necrosis. Insulin pretreatment (100 nm for 30 min) prevented the POA-induced Ca(2+) overload, ATP depletion, inhibition of the PMCA, and necrosis. Moreover, the insulin-mediated protection of the POA-induced Ca(2+) overload was partially prevented by the phosphoinositide-3-kinase (PI3K) inhibitor, LY294002. These data provide the first evidence that insulin directly protects pancreatic acinar cell injury induced by bona fide pancreatitis-inducing agents, such as POA. This may have important therapeutic implications for the treatment of pancreatitis.
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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.