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Pancreatic malignancy
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Giovanni Morana, Alex Faccinetto, Michele Fusaro
The vast majority of pancreatic neoplasms arise from the exocrine pancreas and most are ductal adenocarcinomas. Tumours derived from the pancreatic acini are rare. Cystic pancreatic lesions arising from the parenchyma or ductal system are seen with increasing frequency because of the steady growth in high-quality cross-sectional imaging and pose a major diagnostic problem for the oncological and abdominal radiologist.
Attributes of Peripheral Dopamine and Dopamine Receptors
Published in Nira Ben-Jonathan, Dopamine, 2020
The exocrine pancreas releases pancreatic juice which is composed of digestive enzymes secreted from exocrine acinar cells, and bicarbonate secreted from the epithelial cells lining small pancreatic ducts. Both play essential roles in the conversion of ingested food into fuel. Nutrients absorbed from the small intestine are processed by the liver. Bile produced in the liver plays an important role in digesting fat. The gallbladder concentrates the bile, stores it, and releases it into the small intestines.
The abdomen
Published in Peter Kopelman, Dame Jane Dacre, Handbook of Clinical Skills, 2019
Peter Kopelman, Dame Jane Dacre
The most common movements of the small intestine are non-propulsive segmenting contractions whose main function is to mix the intestinal contents. Peristaltic waves propel food along the lumen. The rate of passage through the duodenum is rapid, while the rate of transit in the ileum may be slow. The ileocaecal valve may further delay the passage of the contents in the ileum, facilitating the absorption of water and some nutrients. The exocrine pancreas secretes an aqueous juice with a high bicarbonate concentration, as well as enzymic fluid containing the major proteolytic enzymes of digestion (trypsin, chymotrypsin and carboxypeptidase), amylase and lipase. This secretion is controlled both by neural and hormonal mechanisms (secretin and cholecystokinin).
Molecular mechanism analysis of m6A modification-related lncRNA-miRNA-mRNA network in regulating autophagy in acute pancreatitis
Published in Islets, 2022
Xiang Li, Hong Qin, Ali Anwar, Xingwen Zhang, Fang Yu, Zheng Tan, Zhanhong Tang
The current paradigm is that pancreatitis initiates in injured acinar cells, the primary exocrine pancreas cell type.5 The data indicate that disordered acinar cell autophagy has been implicated in AP initiation.6 Autophagy is the major catabolic process by which cells eliminate damaged, defective, or unwanted cytoplasmic organelles, long-lived proteins, and lipids and recycle their constituents for energy and biogenesis needs.7 In particular, genetic ablation of the essential autophagy proteins in pancreatic epithelial cells caused spontaneous pancreatitis in mice.8,9 Collectively, maintenance of efficient autophagy in acinar cells plays an important protective role against the onset and progression of pancreatitis, but the specific mechanism is not very clear. Exploring the upstream regulation mechanism of autophagy-related proteins may be a meaningful direction.
Post-pancreatitis diabetes mellitus: investigational drugs in preclinical and clinical development and therapeutic implications
Published in Expert Opinion on Investigational Drugs, 2021
Post-pancreatitis diabetes mellitus (PPDM) is an exemplar secondary diabetes [2]. It develops following an attack of pancreatitis – the most common disease of the exocrine pancreas [3,4]. There has been a fundamental shift in our understanding of the pathogenesis of PDDM over the past quinquennium [2]. While insulin deficiency (as a result of vast mechanical β-cell destruction following extensive pancreatic necrosis or advanced chronic pancreatitis) was thought to be the only underlying mechanism of PPDM, it is now appreciated that the inflammatory process in the exocrine pancreas should not necessarily be massive to set the endocrine pancreas on the path to diabetes and there are several pathways other than β-cell destruction that are involved in the pathogenesis of PPDM [5]. Making some of the pathways druggable targets will offer opportunities to lessen the burden of PPDM and expand the glucose-lowering pharmaceutical armamentarium.
Duration-dependent effects induced by titanium dioxide nanoparticles on pancreas of adult male albino rats (histological and biochemical study)
Published in Ultrastructural Pathology, 2020
Sara M. Abdel Aal, Samah M. Ahmed, Shaimaa Ali Abdelrahman, Abeer A. Abdelrahman, Walaa Samy
Serological results of the present study also proved a significant deficiency in serum α-amylase and lipase activity levels which could be explained by two mechanisms: (1) damaged pancreatic acinar cells which was proved by histopathological examination, (2) secondary to deficient insulin secretion. Barreto et al.52 declared that insulin affects amylase secretion via islet acinar cell axis. It binds with its receptors on acinar cells and stimulates amylase secretion. In another study,53 streptozotocin-diabetic rats showed a reduction of 66% in amylase and 43% in lipase in pancreatic tissue homogenates. The enzyme levels approximated control values after in-vivo insulin administration. It was observed that the hormones like insulin and glucagon affect the enzyme synthesis and release from the exocrine pancreas. Insulin has a trophic effect on the acinar cells, while glucagon has an inhibitory effect. This means that deficiency of insulin and the excess of glucagon in diabetes lead to decreased secretions of amylase and lipase of the exocrine pancreas.54