Histopathology and ex vivo insulin secretion of pancreatic islets in gestational diabetes: A case report

• Published in: Islets 2011-09, Vol.3 (5), p.231-233
• Main Authors: Tancredi, Mariella, Marselli, Lorella, Lencioni, Cristina, Masini, Matilde, Bugliani, Marco, Suleiman, Mara, Masiello, Pellegrino, Boggi, Ugo, Filipponi, Franco, Dotta, Francesco, Marchetti, Piero, Di Cianni, Graziano
• Format: Article
• Language: English
• Subjects: Acinar Cells - metabolism; Acinar Cells - pathology; Adult; Apoptosis - physiology; Arginine - pharmacology; Binding; Biology; Bioscience; Calcium; Cancer; Cell; Cycle; Diabetes, Gestational - metabolism; Diabetes, Gestational - pathology; Fatal Outcome; Female; Glucose - pharmacology; Glyburide - pharmacology; Humans; Hypoglycemic Agents - pharmacology; Insulin - metabolism; Insulin Secretion; Islets of Langerhans - drug effects; Islets of Langerhans - metabolism; Islets of Langerhans - pathology; Landes; Organ Culture Techniques; Organogenesis; Pregnancy; Proteins
• ISSN: 1938-2014; 1938-2022
• DOI: 10.4161/isl.3.5.15940

Gestational diabetes (GD) results from insufficient endogenous insulin supply. No information is available on features of islet cells in human GD. Herein, we describe several properties of islets from a woman with GD. Immunohistochemical stainings and EM analyses were performed on pancreatic samples. Islet isolation was achieved by enzymatic dissociation and density gradient centrifugation. Ex vivo insulin secretion was studied in response to fuel secretagogues. Control islets were obtained from matched non-pregnant, non-diabetic women. Total insulin positive area was lower in GD, mainly due to the presence of smaller islets. β-cell apoptosis and the presence of Ki67 positive islet cells were similar in GD and controls, whereas the amount of insulin positive cells in or close to the ducts was decreased in GD. Ex vivo insulin secretion did not differ between GD and non-pregnant, non-diabetic islets. These findings suggest that in this case of human GD there might mainly be a defect of β-cell amount, not due to increased apoptosis, but possibly to insufficient regeneration.