Purpose Of Review: To summarize advances and limitations in pancreas procurement and preservation for pancreas and islet transplantation, and review advances in islet protection and preservation.
Recent Findings: Pancreases procured after cardiac death, with in-situ regional organ cooling, have been successfully used for islet transplantation. Colloid-free Celsior and histidine-tryptophan-ketoglutarate preservation solutions are comparable to University of Wisconsin solution when used for cold storage before pancreas transplantation. Colloid-free preservation solutions are inferior to University of Wisconsin solution for pancreas preservation prior to islet isolation and transplantation. Clinical reports on pancreas transplants suggest that the two-layer method may not offer significant benefits over cold storage with the University of Wisconsin solution: improved oxygenation may depend on the graft size; benefits in experimental models may not translate to human organs. Improvements in islet yield and quality occurred from pancreases treated with inhibitors of stress-induced apoptosis during procurement, storage, isolation or culture desirable before islet isolation and transplantation and may improve islet yield and quality. Methods for real-time, noninvasive assessment of pancreas quality during preservation have been implemented and objective islet-potency assays have been developed and validated. These innovations should contribute to objective evaluation and establishment of improved pancreas-preservation and islet-isolation strategies.
Summary: Cold storage may be adequate for preservation before pancreas transplants, but insufficient when pancreases are processed for islets or when expanded donors are used. Supplementation of cold-storage solutions with cytoprotective agents and perfusion may improve pancreas and islet transplant outcomes.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1097/MOT.0b013e3282f63942 | DOI Listing |
Acta Physiol (Oxf)
February 2025
UR Diabète et Thérapeutiques, Centre européen d'étude du Diabète, Université de Strasbourg, Strasbourg, France.
Aim: Pancreatic β-cells are susceptible to inflammation, leading to decreased insulin production/secretion and cell death. Previously, we have identified a novel triceps-derived myokine, DECORIN, which plays a pivotal role in skeletal muscle-to-pancreas interorgan communication. However, whether DECORIN can directly impact β-cell function and susceptibility to inflammation remains unexplored.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, Trondheim, 7028, Norway.
Enteroviruses can infect various human organs, causing diseases such as meningitis, the common cold, hand-foot-and-mouth disease, myocarditis, pancreatitis, hepatitis, poliomyelitis, sepsis, and type 1 diabetes. Currently, there are no approved treatments for enterovirus infections. In this study, we identified a synergistic combination of orally available, safe-in-man pleconaril, AG7404, and mindeudesivir, that at non-toxic concentrations effectively inhibited enterovirus replication in human cell and organoid cultures.
View Article and Find Full Text PDFFront Surg
January 2025
Department of Abdominal Transplant and Hepatopancreatobiliary Surgery, Nationwide Children's Hospital, Columbus, OH, United States.
Background: Prepancreatic postduodenal portal vein (PPPV) is a rare anatomic variant where the portal vein (PV) runs anterior to the pancreas and posterior to the duodenum. Only 20 cases of PPPV, all in adults, have been reported in literature. We report the first case of PPPV in a pediatric patient discovered intraoperatively during total pancreatectomy with islet autotransplantation (TPIAT) and the third known case in which the PPPV could be isolated intraoperatively.
View Article and Find Full Text PDFDiabetes Metab J
January 2025
Department of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.
Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation.
View Article and Find Full Text PDFAm J Transplant
January 2025
Division of Endocrinology, Diabetes, Metabolism & Nutrition, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Treating acute rejection of a pancreas transplant in a severely immunocompromised patient with viral opportunistic infection is challenging due to the balance of rescuing from rejection without worsening the morbidity of infection and prolonging the infection episode. We present a case involving a pancreas-after-kidney transplant in a patient with CMV high-risk discordance (donor positive/recipient negative) and chronic lymphopenia who developed difficult-to-treat CMV disease approximately six months after pancreas transplant. Following the withdrawal of the antimetabolite due to the persistent CMV DNAemia and lymphopenia, the patient experienced acute pancreas rejection without adequate and sustained response to treatment with steroids and Thymoglobulin.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!