title: Animal models of type 2 diabetes with reduced pancreatic beta-cell mass.
abstract: Type 2 diabetes is increasingly viewed as a disease of insulin deficiency due not only to intrinsic pancreatic beta-cell dysfunction but also to reduction of beta-cell mass. It is likely that, in diabetes-prone subjects, the regulated beta-cell turnover that adapts cell mass to body's insulin requirements is impaired, presumably on a genetic basis. We still have a limited knowledge of how and when this derangement occurs and what might be the most effective therapeutic strategy to preserve beta-cell mass. The animal models of type 2 diabetes with reduced beta-cell mass described in this review can be extremely helpful (a) to have insight into the mechanisms underlying the defective growth or accelerated loss of beta-cells leading to the beta-cell mass reduction; (b) to investigate in prospective studies the mechanisms of compensatory adaptation and subsequent failure of a reduced beta-cell mass. Furthermore, these models are of invaluable importance to test the effectiveness of potential therapeutic agents that either stimulate beta-cell growth or inhibit beta-cell death.
authors.affiliation: Dipartimento di Patologia Sperimentale, Biotecnologie Mediche, Infettivologia ed Epidemiologia, University of Pisa, Scuola Medica, Italy. p.masiello@med.unipi.it
authors.forename: Pellegrino
authors.initials: P
authors.lastname: Masiello
mesh_terms: D000818:Animals; D017362:Cyclic AMP Response Element-Binding Protein / Q000235:genetics; D056742:Cyclin D2; D051358:Cyclin-Dependent Kinase 4 / Q000172:deficiency; D016213:Cyclins / Q000172:deficiency; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D000077270:Exenatide; D005317:Fetal Growth Retardation / Q000503:physiopathology; D018398:Homeodomain Proteins; D055504:Insulin Receptor Substrate Proteins; D050417:Insulin-Secreting Cells / Q000473:pathology*; D047908:Intracellular Signaling Peptides and Proteins; D051379:Mice; D008822:Mice, Transgenic; D010455:Peptides / Q000627:therapeutic use; D010750:Phosphoproteins / Q000172:deficiency; D051057:Proto-Oncogene Proteins c-akt / Q000172:deficiency; D051381:Rats; D011972:Receptor, Insulin; D038762:Ribosomal Protein S6 Kinases, 70-kDa / Q000172:deficiency; D015534:Trans-Activators / Q000172:deficiency; D014688:Venoms / Q000627:therapeutic use; D019892:eIF-2 Kinase / Q000172:deficiency
chemical_list: D017362:Cyclic AMP Response Element-Binding Protein; D056742:Cyclin D2; D051358:Cyclin-Dependent Kinase 4; D016213:Cyclins; D000077270:Exenatide; D018398:Homeodomain Proteins; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; D010455:Peptides; D010750:Phosphoproteins; D051057:Proto-Oncogene Proteins c-akt; D011972:Receptor, Insulin; D038762:Ribosomal Protein S6 Kinases, 70-kDa; D015534:Trans-Activators; D014688:Venoms; D019892:eIF-2 Kinase; C486196:Ccnd2 protein, mouse; C526298:Irs2 protein, mouse; C526299:Irs2 protein, rat; C084010:pancreatic and duodenal homeobox 1 protein