The pancreatic gland secretes most of the enzymes and many other macromolecules needed for food digestion in the gastrointestinal tract. These molecules play an important role in digestion, host defense and lubrication. The secretion of pancreatic proteins ensures the availability of the correct mix of proteins when needed. This review describes model systems available for the study of the econobiology of secretory granule content. The secretory pancreatic molecules are stored in large dense-core secretory granules that may undergo either constitutive or evoked secretion, and constitute the granule inventory of the cell. It is proposed that the Golgi complex functions as a distribution center for secretory proteins in pancreatic acinar cells, packing the newly formed secretory molecules into maturing secretory granules, also known functionally as condensing vacuoles. Mathematical modelling brings forward a process underlying granule inventory maintenance at various physiological states of condensation and aggregation by homotypic fusion. These models suggest unique but simple mechanisms accountable for inventory buildup and size, as well as for the distribution of secretory molecules into different secretory pathways in pancreatic acinar cells.
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http://dx.doi.org/10.1016/j.acthis.2015.11.011 | DOI Listing |
BMC Pediatr
January 2025
Department of Pediatric, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Background: Pediatric pancreatic acinar cell carcinoma (PACC) is an exceptionally rare and poorly understood malignancy with a challenging prognosis. Its clinical presentation is often atypical, and standardized treatment guidelines are currently unavailable. While genetic alterations in adult PACC have been studied to some extent, knowledge of genetic abnormalities in pediatric cases remains limited.
View Article and Find Full Text PDFPharmacol Res
January 2025
Department of Integrated Traditional Chinese and Western Medicine, West China Hospital of Sichuan University, Chengdu, China. Electronic address:
The necrosis of pancreatic acinar cells is a key molecular event in the progression of acute pancreatitis (AP), with disturbances in mitochondrial energy metabolism considered to be a direct causative factor of acinar cell necrosis. Histidine triad nucleotide-binding protein 2 (HINT2) has been implicated in the development of various diseases, whereas its involvement in the progression of AP remains unclear. This study aims to investigate the role of HINT2 in AP.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Translational Research and Cellular Therapeutics, Arthur Riggs Diabetes and Metabolism Research Institute, Duarte, USA.
Lectins are produced in almost all life forms, can interact with targets (glycans) in a cross-kingdom manner and have served as valuable tools for studying glycobiology. Previously, a bacterial lectin, named Streptomyces hemagglutinin (SHA), was found to agglutinate human type B erythrocytes. However, the binding of SHA to mammalian cell types other than human erythrocytes has not been explored.
View Article and Find Full Text PDFFront Nutr
January 2025
Department of Ultrasound, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.
Background: Hyperuricemia and non-alcoholic fatty pancreas disease (NAFPD) are prevalent metabolic diseases, but the relationship between them remains underexplored.
Methods: Eighteen Sprague-Dawley rats were randomly assigned to three groups: normal (CON), high-fat (PO), and high-fat high-uric acid (PH). After 12 weeks, serum uric acid (SUA) and triacylglycerol levels were measured.
Ann Surg Treat Res
January 2025
Center for Liver and Pancreatobiliary Cancer, National Cancer Center, Goyang, Korea.
Purpose: This study investigated epidemiologic features of patients with pancreatic cancer in Korea, according to the histologic subtypes.
Methods: The Korea Central Cancer Registry data on patients with pancreatic cancer from 1999 to 2019 were reviewed. The 101,446 patients with pancreatic cancer (C25 based on the International Classification of Diseases, 10th revision) were allocated according to the following morphological codes: A, endocrine; B, carcinoma excluding cystic and mucinous; C, cystic or mucinous; D, acinar cell; and E, sarcoma and soft tissue tumor.
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