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Gestational high-fat programming impairs insulin release and reduces Pdx-1 and glucokinase immunoreactivity in
Marlon E Cerf1, Charna S Chapman, Christo J Muller
1Diabetes Discovery Platform, Medical Research Council, Tygerberg, Cape Town, South Africa. marlon.cerf@mrc.ac.za
Insights
Gestational high-fat diets impair neonatal rat insulin release and reduce Pdx-1 and glucokinase (GK) protein levels. These findings link maternal diet to beta-cell dysfunction and altered glucose regulation in offspring.
Area of Science:
- Endocrinology
- Developmental Biology
- Nutritional Science
Background:
- Gestational high-fat diets are linked to neonatal hyperglycemia and impaired beta-cell development.
- Understanding the mechanisms behind these programming effects is crucial for preventing metabolic disorders.
Purpose of the Study:
- To investigate if gestational high-fat programming alters insulin release and the immunoreactivity of key beta-cell proteins (Pdx-1, glucokinase, GLUT-2) in neonates.
- To determine the impact of maternal high-fat diet on pancreatic islet function and gene/protein expression.
Main Methods:
- Neonatal rats were exposed to either a standard or high-fat diet in utero.
- Insulin release from isolated islets was measured at various glucose concentrations.
- Quantitative polymerase chain reaction and immunohistochemistry were used to assess Pdx-1, glucokinase (GK), and glucose transporter (GLUT)-2 expression and immunoreactivity.
Main Results:
- High-fat-programmed neonates exhibited reduced insulin release at higher glucose concentrations (13 and 22 mmol/L).
- No significant differences were observed in Pdx-1, GK, or GLUT-2 messenger RNA expression between groups.
- Immunoreactivity for Pdx-1 and GK was significantly reduced in high-fat-programmed neonates, while GLUT-2 showed a nonsignificant reduction.
Conclusions:
- Gestational high-fat programming impairs neonatal rat insulin secretion capacity.
- Reduced Pdx-1 and GK immunoreactivity suggests altered protein expression, contributing to beta-cell dysfunction.
- Maternal diet during gestation significantly impacts offspring pancreatic islet function and glucose homeostasis.
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.
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