Cortisone-induced islet cell hyperplasia in hamsters.
Pancreatic islet cell hyperplasia was studied in hamsters during one to eight weeks of cortisone treatment. Measurement of serum glucose and insulin; pancreatic insulin, glucagon, somatostatin, pancreatic polypeptide as well as islet tissue morphometry were performed. Serum glucose was highest at week 2, followed by mild to moderate hyperglycemia. Serum insulin was increasingly higher from week 1 to week 8. Pancreatic insulin was maximal at week 5 then declined through week 8 in the presence of beta cell neurosis in markedly hyperplastic islets. Pancreatic concentration of somatostatin and pancreatic polypeptide moderately increased more than the control levels; however, compared with the controls, glucagon was reduced by cortisone treatment. Effect of cortisone in the four types of islet cells is discussed, particularly on beta cell hyperplasia, which appears to be a response to decreased insulin binding to the target organs with no changes in receptor concentration.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003348:Cortisone / Q000494:pharmacology*; D006224:Cricetinae; D005260:Female; D005934:Glucagon / Q000032:analysis; D006965:Hyperplasia; D007328:Insulin / Q000032:analysis / Q000097:blood; D007515:Islets of Langerhans / Q000187:drug effects* / Q000473:pathology; D008647:Mesocricetus; D010179:Pancreas / Q000032:analysis; D010191:Pancreatic Polypeptide / Q000032:analysis; D013004:Somatostatin / Q000032:analysis; D013997:Time Factors
D001786:Blood Glucose; D007328:Insulin; D013004:Somatostatin; D010191:Pancreatic Polypeptide; D005934:Glucagon; D003348:Cortisone