PMID: 6987319Apr 1, 1980Paper

Iron nitrilotriacetate--induced experimental diabetes in rats

The Journal of Laboratory and Clinical Medicine
M E MayM G Buse

Abstract

The etiology of diabetes in some conditions of iron overload is not known. We studied growth, glucose tolerance, and pancreatic islet cell morphology and cytochemistry in rats administered parenteral FeNTA. These rats developed glucosuria, slowing of growth with eventual weight loss, polyuria, polydipsia, and death. They had normal fasting plasma glucose levels but decreased glucose tolerance and insulin response to glucose. Although no Prussian blue staining of iron was observed in pancreatic islets by light microscopy, at the ultrastructural level insulin-secreting beta-cells showed ferrin iron deposits localized to the plasmalemma and the cytoplasmic surface of secretory granule membranes. Prussian blue staining was also observed in parenchymal cells of the liver, heart, and kidney, in order of decreasing intensity. Animals treated with an equivalent dose of NTA, saline, or iron-dextran in saline had normal growth and response to glucose and did not exhibit pancreatic iron deposits at the light or ultrastructural level. These results support the hypothesis that iron affects pancreatic islet cell function and may be an etiologic agent of diabetes mellitus in hemochromatosis.

Related Concepts

Acetic Acids
Blood Glucose
Streptozotocin Diabetes
Ferrocyanides
Intravenous Glucose Tolerance Test
Iron
Islets of Langerhans
Kidney
Liver
Trisodium Nitrilotriacetate

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