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. beta-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 beta-cell amount, not due to increased apoptosis, but possibly to insufficient regeneration.

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

TANCREDI, MARIELLA;MARSELLI, LORELLA;LENCIONI, CRISTINA;MASINI, MATILDE;BUGLIANI, MARCO;MASIELLO, PELLEGRINO;BOGGI, UGO;FILIPPONI, FRANCO;MARCHETTI, PIERO;
2011-01-01

Abstract

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. beta-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 beta-cell amount, not due to increased apoptosis, but possibly to insufficient regeneration.
2011
Tancredi, Mariella; Marselli, Lorella; Lencioni, Cristina; Masini, Matilde; Bugliani, Marco; Suleiman, M; Masiello, Pellegrino; Boggi, Ugo; Filipponi, Franco; Dotta, F; Marchetti, Piero; DI CIANNI, G.
File in questo prodotto:
File Dimensione Formato  
Islets 2011.pdf

solo utenti autorizzati

Tipologia: Versione finale editoriale
Licenza: Importato da Ugov Ricerca - Accesso privato/ristretto
Dimensione 569.72 kB
Formato Adobe PDF
569.72 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/199955
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? 1
  • Scopus 7
  • ???jsp.display-item.citation.isi??? 6
social impact