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Objective: To establish a rat model of chronic pancreatitis, and to prove the activation of sonic hedgehog (SHH) signaling pathways in chronic pancreatitis.
Methods: This study was conducted between January and July 2008 in the Department of General Surgery, Wuhan General Hospital, Guangzhou Military Command, Wuhan, China. Thirty Wistar rats were randomly divided into 3 groups: control group (A), experimental control group (B), and model group (C) (10 rats in each group). Trinitrobenzene sulfonic acid was infused into the pancreatic duct to induce chronic pancreatitis in the model group rats. In the experimental control group, we opened the abdominal cavity and infused with 0.9% sodium chloride solution. Serum levels of bilirubin and amylase were determined by radioimmunoassay. Histopathological alterations were studied using the optical microscopy. Expression of patched-1 (PTCH-1), smoothened (SMO), and SHH were detected by immunohistochemistry.
Results: Compared with the control group (A), the serum bilirubin and amylase in the model group increased significantly after 7 days of treatment, and fibrotic proliferation of pancreatic tissues were found after 35 days; the expression of PTCH-1, SMO, and SHH in the pancreatic tissue increased significantly in the model group.
Conclusion: Trinitrobeneze sulfonic acid can induce chronic pancreatitis in rat. The SHH signaling pathway is activated in rats with chronic pancreatitis.
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United European Gastroenterol J
September 2025
Department of Gastroenterology and Hepatology, St. Antonius Hospital, Nieuwegein, the Netherlands.
Diabetes Obes Metab
September 2025
Centre for Pancreatic Diseases and Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark.
Aims: Population-based studies have consistently shown that individuals with diabetes secondary to chronic pancreatitis (pancreatic diabetes) have a high risk of hypoglycaemia. We aimed to investigate whether this risk has declined over recent years following the introduction of modern glucose-lowering medications.
Materials And Methods: In this Danish nationwide population-based cohort study, we included all adults with new-onset diabetes between 1998 and 2022 and classified them as having pancreatic diabetes, type 1, or type 2 diabetes.
J Surg Case Rep
September 2025
Department of Surgery, Faculty of Medicine, University of Colombo, No. 25, Kynsey Road, Colombo 8, Sri Lanka.
Pancreatogastric fistulas are rare but serious complications of chronic pancreatitis that can lead to life-threatening gastrointestinal bleeding due to erosion of nearby blood vessels. We present a case of a 43-year-old man with chronic calcific pancreatitis and a history of alcohol misuse, who experienced recurrent hematemesis and melena over 2 months. Despite multiple endoscopies and transfusions, the bleeding source remained unidentified until imaging revealed a fistulous tract between the pancreas and the posterior gastric wall.
View Article and Find Full Text PDFExp Cell Res
September 2025
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300100, China; Institute of Integrative Medicine for Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100,
The characteristic pathological change in chronic pancreatitis (CP) is pancreatic fibrosis. In the early stages of CP development, injured acinar cells induce the infiltration of inflammatory cells, followed by pancreatic stellate cell (PSC) activation. Activated PSC induce the deposition of extracellular matrix (ECM) and promote the development of pancreatic fibrosis.
View Article and Find Full Text PDFObesity is a known risk factor for diseases of the pancreas, including diabetes, pancreatic cancer and pancreatitis, but mechanisms remain unclear. To elucidate how obesity impacts pancreatic immune homeostasis, we performed spatial, transcriptomic and functional profiling of human pancreatic immune cells from obese and non-obese organ donors. Obesity was associated with higher density of tissue resident memory T-cells (TRM) in the exocrine pancreas which display high cytotoxic functions and aggregated around macrophages.
View Article and Find Full Text PDF