Journal Article10.1111/J.1440-1827.1989.TB01495.X
Pancreatic islets after repeated injection of Fe3+-NTA. An ultrastructural study of diabetic rats.
16
TL;DR: Repeated venesection therapy of rats injected with Fe3+‐NTA for 120 days resulted in an increase of morphologically normal B cells with a smaller number of necrotizing cells, accompanied by recovery from diabetic symptoms, and the toxic effect of injected iron on B cells was clarified.
read more
Abstract: Pancreatic islet cells were examined ultrastructurally in rats after repeated intraperitoneal injections of ferric nitrilotriacetate (Fe3+- NTA) to produce a model of bronze diabetes. Despite diabetic signs such as glycosuria and ketouria, no ultrastructural alterations were found in islet cells up to 90 days after the beginning of the Fe3+-NTA injections. After 120 days, however, degenerative changes appeared, with most B cells of the islets of Langerhans showing clumped nuclear chromatin, a dilated nuclear envelope, vacuolated and dilated endoplasmic reticulum, and a loss of cell polarization toward the capillary lumen. The cells contained a number of light secretory granules with an electron-lucent core and a narrow halo. Numerous electron-dense ferritin-like particles were also found in the cytoplasmic matrix, and A and D cells were almost intact. Repeated venesection therapy of rats injected with Fe3+-NTA for 120 days resulted in an increase of morphologically normal B cells with a smaller number of necrotizing cells. This process was accompanied by recovery from diabetic symptoms. The toxic effect of injected iron on B cells was thus clarified.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Role of Iron Deficiency and Overload in the Pathogenesis of Diabetes and Diabetic Complications
TL;DR: This review will first outline iron homeostasis, function, and toxicity, and then mainly summarize the data regarding the roles of iron deficiency and overload in the pathogenesis of diabetes and diabetes complications, as well as the possible links of iron to diabetes and diabetic complications.
152
Iron Regulation of Pancreatic Beta-Cell Functions and Oxidative Stress.
Marie Balslev Backe,Ingrid Wahl Moen,Christina Ellervik,Jakob Bondo Hansen,Thomas Mandrup-Poulsen +4 more
TL;DR: It is proposed that clinical trials are warranted to clarify the impact of dietary or pharmacological iron reduction on the development of metabolic disorders.
102
Transferrin Receptor Expression in Normal, Iron‐deficient and Iron‐overloaded Rats
TL;DR: It is concluded that TfR expression is negatively regulated by the tissue concentration of iron.
49
Iron Metabolism in Pancreatic Beta-Cell Function and Dysfunction.
TL;DR: In this paper, the authors provide insights into the mechanisms responsible for iron homeostasis in pancreatic beta-cells, describing how alteration of these processes has been related to beta-cell damage and failure.
Genome-linked toxic responses to dietary iron overload
Paul Whittaker,Virginia C. Dunkel,Thomas J. Bucci,Donna F. Kusewitt,J. Dale Thurman,Alan Warbritton,George L. Wolff +6 more
TL;DR: Genome-related differences to Fe overload between and within rodent species were evaluated in the present study and PCNA assays showed significant stimulatory effects of the high dose of Fe on hepatocyte proliferation in the F344 rats and the C5YSF, mice but not in the B6C3f, mice.
32
References
The Kinetics and Mechanism of Iron (III) Exchange between Chelates and Transferrin IV. THE REACTION OF TRANSFERRIN WITH IRON(III) NITRILOTRIACETATE
George W. Bates,Joachim Wernicke +1 more
TL;DR: The reaction of iron(III)-nitrilotriacetate (NTA) with transferrin was studied with a stopped flow spectrophotometer and a reaction sequence is proposed.
173