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Exposure to binge ethanol and fatty acid ethyl esters exacerbates chronic ethanol-induced pancreatic injury in hepatic alcohol dehydrogenase-deficient deer mice

Mukund P. Srinivasan, Kamlesh K. Bhopale, Anna A. Caracheo, Lata Kaphalia, Bin Gong, Vsevolod L. Popov, Paul J. Boor, G.A.S. Ansari, Bhupendra S. Kaphalia

2022American Journal of Physiology-Gastrointestinal and Liver Physiology12 citationsDOIOpen Access PDF

Abstract

We established a chronic EtOH feeding model of hepatic alcohol dehydrogenase-deficient (ADH − ) deer mice, which mimics several fibroinflammatory features of human alcoholic chronic pancreatitis (ACP). The fibroinflammatory and morphological features exacerbated by chronic plus binge EtOH and FAEEs exposure provide a strong case for metabolic basis of ACP. Most importantly, several pathological and molecular targets identified in this study provide a much broader understanding of the mechanism and avenues to develop therapeutics for ACP.

Topics & Concepts

EndocrinologyInternal medicineOxidative stressAlcohol dehydrogenasePancreasChemistryEthanolAcinar cellLiquid dietImmunostainingMedicineBiochemistryImmunohistochemistryPancreatitis Pathology and TreatmentLiver Disease Diagnosis and TreatmentPancreatic function and diabetes
Exposure to binge ethanol and fatty acid ethyl esters exacerbates chronic ethanol-induced pancreatic injury in hepatic alcohol dehydrogenase-deficient deer mice | Litcius