Animal models replicating human famine conditions have been developed to enable a more in-depth investigation of maternal calorie restriction throughout pregnancy and the long-term health consequences that this nutritional insult imposes on the developing offspring. Various animal species have been utilized whilst studying the fetal origins of adult metabolic disease in response to maternal feed restriction using dietary insults of up to 70% ad libitum food restriction.
Maternal total food restriction (50% of normal food intake) in the rat throughout the gestation period can induce intrauterine growth restriction and result in significantly reduced birth weight. This poor fetal growth is then accompanied by numerous metabolic disturbances in later life. Compared to age-matched control rat offspring, the blood pressure of the maternal food-restriction offspring is significantly elevated and endothelial vascular dysfunction is evident. Insulin resistance, as defined by an elevated fasting plasma insulin level, has also been shown in adult rats exposed in utero to the adverse effects of severe maternal food restriction (to only 30% of ad libitum intake). In guinea pigs, mild to moderate maternal food restriction (70%-85% ad libitum intake) during the pregnancy leads to perturbations in postnatal glucose-insulin homeostasis as well as alterations in the homeostasis of cholesterol metabolism in the male offspring.
Despite the observed significant reduction in birth weight, adult rats exposed to maternal undernutri-tion (30% of ad libitum intake) whilst in utero have been shown to develop obesity. Compared to the control offspring, the feed-restricted offspring appear to have been inappropriately programed and display hyperphagia and elevated food consumption as a consequence of in utero exposure to an adverse maternal diet. The underlying mechanisms leading to the hyperphagia in these offspring remains to be determined. However, the involvement of leptin resistance has been implied as these offspring also display hyperleptinemia and have significantly elevated fat pad mass as adults.
Even short-term maternal food restriction during the various stages of the gestational period has been demonstrated to provoke perturbations within the metabolic processes of the offspring. Exposure to maternal malnutrition, particularly in the final trimester and during lactation, impairs the programming of /3-cell development and induces alterations in the fetal endocrine pancreas that persist into adulthood such that the offspring at 12 months of age display profound insulinopenia and marked glucose intolerance.
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