Gestational high-fat programming impairs insulin release and reduces Pdx-1 and glucokinase immunoreactivity in neonatal Wistar rats.
Metabolism
; 58(12): 1787-92, 2009 Dec.
Article
en En
| MEDLINE
| ID: mdl-19604517
ABSTRACT
Hyperglycemia and compromised beta-cell development were demonstrated in neonatal rats programmed with a gestational high-fat diet. The aim of this study was to determine whether these changes were attributed to impaired insulin release and altered immunoreactivity of Pdx-1, glucokinase (GK), and glucose transporter (GLUT)-2 in high-fat-programmed neonates. Fetuses were maintained, via maternal nutrition, on either a standard laboratory diet (control) or a high-fat diet throughout gestation (HFG). Pancreata from 1-day-old neonates were excised for islet isolation and the subsequent measurement of insulin release at 2.8, 6.5, 13, and 22 mmol/L glucose. Other pancreata were either snap frozen for quantitative polymerase chain reaction or formalin fixed for immunohistochemistry followed by image analysis. The HFG neonates had reduced insulin release at 13- and 22-mmol/L glucose concentrations. No significant differences were found in Pdx-1, GK, or GLUT-2 messenger RNA expression. In HFG neonates, immunoreactivity of both Pdx-1 and GK was significantly reduced, with a nonsignificant reduction in GLUT-2. Gestational high-fat programming impairs insulin release and reduces Pdx-1 and GK immunoreactivity.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Preñez
/
Grasas de la Dieta
/
Transactivadores
/
Proteínas de Homeodominio
/
Glucoquinasa
/
Insulina
/
Animales Recién Nacidos
Límite:
Animals
/
Pregnancy
Idioma:
En
Revista:
Metabolism
Año:
2009
Tipo del documento:
Article
País de afiliación:
Sudáfrica