Background: Impaired metabolism and cytosolic Ca 2ϩ overload in pancreatic acinar cells can trigger pancreatitis. Results: Insulin protected cells from oxidant-induced Ca 2ϩ overload, inhibition of the plasma membrane calcium pump (PMCA), and ATP depletion. Conclusion: Insulin switches metabolism toward glycolysis and fuels the PMCA even when mitochondria are impaired. Significance: This mechanism may provide an important therapeutic strategy for pancreatitis.

Background: Palmitoleic acid is a major pancreatitis-inducing agent.Results: Insulin protected cells from palmitoleic acid (POA)-induced ATP depletion, inhibition of the plasma membrane calcium pump (PMCA), cytotoxic Ca2+ overload and necrosis.Conclusion: Insulin protects against acinar cell injury induced by pancreatitis-inducing agents.Significance: This provides an important therapeutic strategy for treating pancreatitis with insulin therapy.

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