An immunohistochemical, ultrastructural, and physiologic study of pancreatic islets from copper-deficient, penicillamine-treated rats.
Murine copper deficiency induced by diet and supplemented with a copper chelator is known to produce a progressive atrophy of pancreatic acinar tissue largely replaced by noninflammatory lipomatosis, while the ductal and endocrine systems appear to remain unaffected. The islets were studied morphologically and physiologically in animals rendered copper deficient by diet and supplemented with D-penicillamine. Using immunohistochemistry, the distribution of islet cell types from copper-deficient animals exhibited a normal cellular complement for A-, B-, D-, and PP-cells. Ultrastructural analysis showed the islet tissue remains normal in appearance during the course of the metal-deficient state. Physiologic data based on the response of islets to a low- and high-glucose load in perfused, isolated pancreata as well as intravenous glucose tolerance tests indicated that insulin-secreting B-cells were functionally normal. Because of the accessibility of islets enhanced by atrophy of acini, this model may be adopted for the isolation of viable islets and for in situ physiologic studies of islet hormone secretion.
Weaver
C
C
Sorenson
R L
RL
Kaung
H L
HL
D000818:Animals; D003300:Copper / Q000172:deficiency*; D005260:Female; D005934:Glucagon / Q000378:metabolism; D005951:Glucose Tolerance Test; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D010191:Pancreatic Polypeptide / Q000378:metabolism; D010396:Penicillamine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000378:metabolism
D007328:Insulin; D013004:Somatostatin; D010191:Pancreatic Polypeptide; D003300:Copper; D005934:Glucagon; D010396:Penicillamine