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Impact of acute schistosomiasis mansoni and concurrent type 1 diabetes on pancreatic architecture in mice.
Exp Parasitol
January 2025
Romero Lascasas Porto Laboratory of Helminthology, Department of Microbiology, Immunology and Parasitology, Medical Sciences College (FCM), Rio de Janeiro State University (UERJ), Rio de Janeiro, Brazil.
It is not well understood how type 1 diabetes (T1D) and concomitant acute schistosomiasis mansoni affect pancreatic architecture. Male Swiss mice were administered streptozotocin (single 100 mg/kg i.p.
View Article and Find Full Text PDFCFTR represses a PDX1 axis to govern pancreatic ductal cell fate.
iScience
December 2024
Department of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
Inflammation, acinar atrophy, and ductal hyperplasia drive pancreatic remodeling in newborn cystic fibrosis (CF) ferrets lacking a functional cystic fibrosis conductance regulator (CFTR) channel. These changes are associated with a transient phase of glucose intolerance that involves islet destruction and subsequent regeneration near hyperplastic ducts. The phenotypic changes in CF ductal epithelium and their impact on islet function are unknown.
View Article and Find Full Text PDFSymptom burden after acute pancreatitis and its correlation with exocrine pancreatic function: A multicenter prospective study.
Clin Transl Gastroenterol
December 2024
Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University, Wexner Medical Center, Columbus, OH, USA.
Background And Aims: Gastrointestinal (GI) symptoms and weight loss develop during and after acute pancreatitis (AP), but remain understudied. In this prospective, multicenter study, we aim to assess GI symptom burden and weight loss and their correlation with exocrine function up to 12-mo post-AP.
Methods: GI symptom burden, anthropometrics, and exocrine pancreatic function were systematically measured in adults (≥18 years) with AP at predefined intervals: hospitalization (enrollment), 3-months (3-mo), and 12-mo post-AP.
Serum exocrine pancreas enzymes are biomarkers of immunotherapy response in new-onset type 1 diabetes.
Front Endocrinol (Lausanne)
December 2024
Division of Endocrinology, Department of Pediatrics, University of Florida, Gainesville, FL, United States.
Introduction: The immune-mediated destruction of insulin-producing β-cells characterizes type 1 diabetes. Nevertheless, exocrine pancreatic enzymes, including amylase, lipase, and trypsin, are also significantly reduced in type 1 diabetes. With an immunotherapy now approved to treat early-stage type 1 diabetes, biomarkers to delineate response to treatment are needed.
View Article and Find Full Text PDFPancreatic endocrine-exocrine crosstalk plays a key role in normal physiology and disease. For instance, endocrine islet beta (β) cell secretion of insulin or cholecystokinin (CCK) promotes progression of pancreatic adenocarcinoma (PDAC), an exocrine cell-derived tumor. However, the cellular and molecular mechanisms that govern endocrine-exocrine signaling in tumorigenesis remain incompletely understood.
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