[Functional and morphological changes in the islands of Langerhans in obesity].
Functional changes in pancreatic islets seen in obese patients were compared with morphological and ultrastructural alterations in islet cells in rats during varying time of the experimental hypothalamic obesity development. The blood level of insulin and C-peptide in obese patients increases with the disease severity, but functional B-cell reserves tend to decrease as shown by glucose tolerance test. Reduction in glucagon release is seen in insulin hypoglycemia. A fall in B cell reserves is caused by their functional overtension, destruction and replacement of the pancreatic parenchyma by the connective tissue. The main morphological reason for glucagon release lowering in patients with pronounced obesity is reduction of A cell number. An elevation of somatostatin level in the blood of obese patients with a simultaneous decrease in D cell number in pancreatic islets of experimental animals indicates that this rise is stipulated by intensified hypothalamic somatostatin secretion.
D000818:Animals; D002096:C-Peptide / Q000378:metabolism; D005934:Glucagon / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000473:pathology / Q000503:physiopathology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D009765:Obesity / Q000473:pathology / Q000503:physiopathology*; D051381:Rats
D002096:C-Peptide; D007328:Insulin; D005934:Glucagon
Funktsional'nye i morfologicheskie izmeneniia ostrovkovogo apparata podzheludochnoĭ zhelezy pri ozhirenii.