Cystic fibrosis transmembrane conductance regulator (CFTR) is a channel and regulator protein that is crucially involved in transepithelial ion transport. In the exocrine pancreas, the CFTR-mediated secretion of an electrolyte-rich fluid is a major but as yet incompletely understood function. We show here that the peptide guanylin is a specific activator of CFTR function in the human pancreas implicating regulation of pancreatic electrolyte secretion. Guanylin and its affiliated signaling and effector proteins including guanylate cyclase C, cGMP-dependent protein kinase II, CFTR, and the epithelial Cl-/HCO3- exchanger, anion exchanger 2, are highly expressed in the human pancreas. Guanylin is localized specifically to the typical centroacinar cells and proximal duct cells which, based on its additional presence in the pancreatic juice, is obviously released luminally into the pancreatic ducts. The guanylin receptor and the respective functional downstream proteins are all confined to the apical membrane of the duct cells implicating an as yet unknown route of luminal regulatory pathway of electrolyte secretion in the ductal system. Functional studies in two different human pancreatic duct cell lines expressing the CFTR Cl- channel that is functionally intact in CAPAN-1 cells but defective (delta F508) in CFPAC-1 cells clearly identify guanylin as a specific regulator of pancreatic CFTR channel function. Whole-cell patch-clamp recordings in CAPAN-1 cells revealed that forskolin induces an increase of Cl- conductance mediated by cAMP. In contrast, guanylin increased Cl- conductance in the same cells via cGMP but not cAMP; the respective membrane current was largely blockable by the sulfonylurea glibenclamide. In CFPAC-1 cells, however, neither guanylin nor forskolin produced a current activation. Based on the present findings we conclude that guanylin is an intrinsic pancreatic regulator of Cl- current activation in pancreatic duct cells via cGMP and CFTR. Remarkably, in the pancreas guanylin may exert its function through an intriguing luminocrine mode via the pancreatic juice.
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http://dx.doi.org/10.1007/s004180000244 | DOI Listing |
Mol Metab
March 2025
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA; Howard Hughes Medical Institute, Dallas, TX, 75390, USA; Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA. Electronic address:
The bi-functional enzyme FicD catalyzes AMPylation and deAMPylation of the endoplasmic reticulum chaperone BiP to modulate ER homeostasis and the unfolded protein response (UPR). Human hFicD with an arginine-to-serine mutation disrupts FicD deAMPylation activity resulting in severe neonatal diabetes. We generated the mFicD mutation in mice to create a pre-clinical murine model for neonatal diabetes.
View Article and Find Full Text PDFSci Adv
March 2025
Cancer Ecosystems Program, Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, Sydney, New South Wales, Australia.
Pancreatic cancer (PC) is a highly metastatic malignancy. More than 80% of patients with PC present with advanced-stage disease, preventing potentially curative surgery. The neuropeptide Y (NPY) system, best known for its role in controlling energy homeostasis, has also been shown to promote tumorigenesis in a range of cancer types, but its role in PC has yet to be explored.
View Article and Find Full Text PDFPLoS One
March 2025
Cell Biology-Inspired Tissue Engineering (cBITE), MERLN Institute for Technology-Inspired Regenerative Medicine, Maastricht University, Maastricht, The Netherlands.
Type 1 diabetic (T1D) patients are life-long dependent on insulin therapy to keep their blood glucose levels under control. An alternative cell-based therapy for exogenous insulin injections is clinical islet transplantation (CIT). Currently the widespread application of CIT is limited, due to risks associated with the life-long use of immunosuppressive drugs to prevent rejection of donor cells.
View Article and Find Full Text PDFRheumatol Int
March 2025
Department of Rheumatology and Connective Tissue Diseases, Medical University, St. Jaczewskiego 8, 20-090, Lublin, Poland.
Pancreatic panniculitis (PP) and arthritis may be extrapancreatic manifestations of pancreatic disease. The triad of pancreatic disease, panniculitis and polyarthritis, described in the literature as the PPP syndrome, is sometimes observed in patients with acute or chronic pancreatitis, pancreatic cancer or neuroendocrine tumors (NETs). We present a 60-year-old man with polyarthritis and clinically aggressive PP of the limbs.
View Article and Find Full Text PDFDiabetologia
March 2025
Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China.
Aims/hypothesis: Fat deposition in the pancreas is implicated in beta cell dysfunction and the progress of type 2 diabetes. However, there is limited evidence to confirm the correlation and explore how pancreatic fat links with beta cell dysfunction in human type 2 diabetes. This study aimed to examine the spatial relationship between pancreatic fat and islets in human pancreases.
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