Author(s): Theys N, Ahn MT, Bouckenooghe T, Reusens B, Remacle C
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Abstract Accumulating evidence has shown that maternal malnutrition increases the risk of metabolic disease in the progeny. We previously reported that prenatal exposure to a low-protein diet (LP) leads to mitochondrial dysfunction in pancreatic islets from adult rodent offspring that could relate physiological and cellular alterations due to early diet. We aim to determine whether mitochondrial dysfunction could be a common consequence of prenatal nutritional unbalances. Pregnant Wistar rats received either a global food restriction (GFR), consisting in the reduction by 50\% of the normal daily food intake, or a high-fat diet (HF) throughout gestation. GFR or HF diet during pregnancy leads to a lack of increase in insulin release and ATP content in response to glucose stimulation in islets from 3-month-old male and female offspring. These similar consequences originated from impairment in either glucose sensing or glucose metabolism, depending on the type of early malnutrition and on the sex of the progeny. Indeed, the glucose transport across β-cell membrane seemed compromised in female HF offspring, since GLUT-2 gene was markedly underexpressed. Additionally, for each progeny, consequences downstream the entry of glucose were also apparent. Expression of genes involved in glycolysis, TCA cycle and oxidative phosphorylations was altered in GFR and HF rats in a sex- and diet-dependent manner. Moreover, prenatal malnutrition affected the regulators of mitochondrial biogenesis, namely, PPAR coactivator 1 alpha (PGC-1α), since its expression was higher in islets from GFR rats. In conclusion, programming of mitochondrial dysfunction is a consequence of maternal malnutrition, which may predispose to glucose intolerance in the adult offspring. Copyright © 2011 Elsevier Inc. All rights reserved.
This article was published in J Nutr Biochem
and referenced in Journal of Diabetes & Metabolism