Abstract

Thyroxine treatment (2000/ug/kg b.wt., for 5 days) induced experimental hyperthyroidism in ob/ob mice. The relation between insulin secretion and metabolism of pancreatic islets was investigated. Thyroxine treatment inhibited glucose-induced insulin secretion from the isolated perfused ob/ob mouse pancreas and reduced total pancreas insulin content. Histological examination of the pancreas revealed islets with well preserved beta cells which appeared to be reduced in size but not in number. Quantitative evaluation showed a decrease of the beta cell area in relation to the total pancreatic parenchyma probably due to reduced islet cell volume. Glucose-induced insulin release from incubated pancreatic islets and insulin content of pancreatic islets were not reduced after thyroxine treatment. ATP content of islets was normal. Glucose oxidation and glucose utilization by islets were increased. Thyroxine treatment suppressed potentiation of glucose-in — duced 45Ca2+ uptake into the lantanum-nondis-placeable pool of islets induced by fasting in control mice.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call