ArticleThe Journal of biological chemistry2012
Insulin protects pancreatic acinar cells from cytosolic calcium overload and inhibition of plasma membrane calcium pump.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Reappraisal of xenobiotic-induced, oxidative stress-mediated cellular injury in chronic pancreatitis: a systematic review.World journal of gastroenterology · 2014Pooled it
- Hypertriglyceridaemia-Associated Acute Pancreatitis: Pathophysiological Insights and Advances in Clinical Management.Biomedicines · 2026Review
- Renalase peptides reduce pancreatitis severity in mice.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Mitochondrial and Cellular Function in Fibroblasts, Induced Neurons, and Astrocytes Derived from Case Study Patients: Insights into Major Depression as a Mitochondria-Associated Disease.International journal of molecular sciences · 2024Article
- The role of high serum triglyceride levels on pancreatic necrosis development and related complications.BMC gastroenterology · 2023Article
- Stress Hyperglycemia Is Independently Associated with Persistent Organ Failure in Acute Pancreatitis.Digestive diseases and sciences · 2022Article
- 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
- 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
- Transient High Pressure in Pancreatic Ducts Promotes Inflammation and Alters Tight Junctions via Calcineurin Signaling in Mice.Gastroenterology · 2018Article
- Calcium signalling in the acinar environment of the exocrine pancreas: physiology and pathophysiology.The Journal of physiology · 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
- Do Animal Models of Acute Pancreatitis Reproduce Human Disease?Cellular and molecular gastroenterology and hepatology · 2017Review
- Insulin protects pancreatic acinar cells from palmitoleic acid-induced cellular injury.The Journal of biological chemistry · 2014Article
- Glycolytic ATP fuels the plasma membrane calcium pump critical for pancreatic cancer cell survival.The Journal of biological chemistry · 2013Article
- Calcium channels and pumps in cancer: changes and consequences.The Journal of biological chemistry · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Acute pancreatitis is a serious and sometimes fatal inflammatory disease of the pancreas without any reliable treatment or imminent cure. In recent years, impaired metabolism and cytosolic Ca(2+) ([Ca(2+)](i)) overload in pancreatic acinar cells have been implicated as the cardinal pathological events common to most forms of pancreatitis, regardless of the precise causative factor. Therefore, restoration of metabolism and protection against cytosolic Ca(2+) overload likely represent key therapeutic untapped strategies for the treatment of this disease. The plasma membrane Ca(2+)-ATPase (PMCA) provides a final common path for cells to "defend" [Ca(2+)](i) during cellular injury. In this paper, we use fluorescence imaging to show for the first time that insulin treatment, which is protective in animal models and clinical studies of human pancreatitis, directly protects pancreatic acinar cells from oxidant-induced cytosolic Ca(2+) overload and inhibition of the PMCA. This protection was independent of oxidative stress or mitochondrial membrane potential but appeared to involve the activation of Akt and an acute metabolic switch from mitochondrial to predominantly glycolytic metabolism. This switch to glycolysis appeared to be sufficient to maintain cellular ATP and thus PMCA activity, thereby preventing Ca(2+) overload, even in the face of impaired mitochondrial function.
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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.