title: Islet hyperplasia in callitrichids.
abstract: Five callitrichids (three common marmosets -Callithrix jacchus -, a black tufted-eared marmoset -C. penicillata-, and a saddle-back tamarin -Saguinus fuscicollis) were diagnosed with islet hyperplasia by histopathology and immunohistochemistry. All were privately-owned, unrelated callitrichids ranging from 2- to 4-year-old. Relevant findings were anorexia (3/5), vomiting (2/5), ptyalism (1/5), polyuria/polydipsia (1/5), respiratory distress (1/5), hyperglycemia (2/3) and glycosuria (1/1); hyperglycemia and glycosuria were associated with pregnancy in a common marmoset and resolved after reducing simple carbohydrates in diet. All five animals died, three of them after few premonitory signs; in two cases, other concurrent diseases unrelated to islet hyperplasia were considered the cause of death. Additional animals from two facilities had high weight (4), physical obesity (3), polyuria/polydipsia/polyphagia/uriposia (1), hyperglycemia (1), and/or glycosuria (2). Pathologic findings in the deceased callitrichids were: islet hyperplasia (5/5); hemosiderosis (5/5); lipomatosis (4/5) of several tissues (atria, 3/5; pancreas, gall bladder, intestine, esophagus, and thyroid, 2/5; liver, 1/5); pancreatic necrosis or steatonecrosis, and/or acute pancreatitis (3/5); and vacuolation of hepatocytes and renal tubular cells most likely consistent with hepatorenal lipidosis (2/5). The islets of Langerhans were more numerous and larger than in a control, and morphologically normal in all cases, except in a common marmoset that had a few cells with a foamy cytoplasm and shrunken hyperchromatic or picknotic nucleus. Insulin (5/5), glucagon (3/5), and somatostatin (3/5) immunohistochemistry revealed that most cells stained positively for insulin diffusely in their cytoplasm (5/5) (staining restricted to the vascular pole of b-cells in the control). These findings suggest that obesity, insulin resistance and/or type II diabetes may be implicated and thus a prospective study on these diseases in callitrichids is necessary to determine their etiopathogenesis.
authors.affiliation: Clínica Exótics and Universitat Autònoma de Barcelona, Barcelona, Spain. cjuansalles@yahoo.com
authors.forename: Carles
authors.initials: C
authors.lastname: Juan-Sallés
authors.forename: Alberto
authors.initials: A
authors.lastname: Marco
authors.forename: José A
authors.initials: JA
authors.lastname: Ramos-Vara
authors.forename: Ana
authors.initials: A
authors.lastname: Resendes
authors.forename: Jarvier
authors.initials: J
authors.lastname: Vergés
authors.forename: Xavier
authors.initials: X
authors.lastname: Valls
authors.forename: Andrés
authors.initials: A
authors.lastname: Montesinos
mesh_terms: D000818:Animals; D000836:Animals, Zoo; D002143:Callitrichinae; D002423:Cause of Death; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology / Q000662:veterinary*; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000662:veterinary; D005260:Female; D006965:Hyperplasia; D007150:Immunohistochemistry; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000473:pathology*; D008297:Male; D008992:Monkey Diseases / Q000473:pathology*; D009765:Obesity / Q000150:complications