Changes induced by sucrose administration upon the morphology and functionof pancreatic islets in the normal hamster

Background This report documents sequential changes in islet morphology (ce ll replication and islet neogenesis) and glucose-induced insulin secretion in young normal male Syrian hamsters. Methods Three-week-old animals received a control standard commercial diet or this diet supplemented with sucrose - 10% (w/v) solution in drinking wat er, a treatment that stimulated pancreatic growth and function - for 5 (C5/ S5) or 21 (C21/S21) weeks. Insulin secretion and content were measured in i solated islets, while several biochemical parameters were assessed in serum . Different morphological features were analysed in the endocrine pancreas by quantitative immunocytochemistry. Results Serum glucose, triglycerides and total cholesterol levels were comp arable among the groups, whereas serum- and pancreatic-insulin levels were higher in the S hamsters. Islets from S21 hamsters released more insulin th an those from C21 animals at all glucose concentrations tested. The volume densities of the total endocrine pancreas (1.9 +/- 0.2 vs 1.2 +/- 0.2; p <0 .02) of the beta-cell subpopulation, the islet number per unit area (2.4 +/ - 0.1 vs 1.2 +/- 0.1; p <0.0004) and the beta-cell mass (4.2 +/- 0.5 vs 2.3 +/- 0.5; p<0.01) were significantly higher in S5 vs C5 animals. Conversely , the islet volume and the number of beta cells/islets were significantly s maller in S5 than in C5 animals. The beta-eel replication rate in S5 hamste rs was 10-fold that of C5 animals. All these parameters had comparable valu es in S21 and C21 animals. We detected cytokeratin-labelled cells located a t the islet periphery (in alpha cells) and among the ductular cells, only i n the S5 hamsters. Conclusions Sucrose administration to young hamsters causes time-dependent pancreatic modifications, with morphological changes (increase in islet- an d in beta-cell mass with incremented beta-cell replication rate and evidenc e of islet neogenesis) occurring at 5 weeks and insulin secretion (increase in insulin sensitivity to glucose) being mainly affected at 21 weeks. This experimental model could prove useful for studying the mechanisms underlyi ng the control of islet-cell population distribution and for developing new strategies in preventing cell damage. Copyright (C) 1999 John Wiley & Sons , Ltd.