Abstract
Pregnancy and fetal development are periods of rapid growth and cell differentiation when mother and offspring are vulnerable to changes. Adverse events during development can be linked to an increased risk in developing metabolic diseases. Growth restriction in utero is associated with the development of obesity, hypertension, and diabetes. In these processes, the liver plays a fundamental role. The aim of this work was to evaluate the effects of a low protein diet in pregnant and lactating mothers on the antioxidant status of the offspring liver. To reproduce real conditions, we used an experimental rat model. Both ROS and the protective antioxidant systems have to work in coordination to reach a state of redox homeostasis. Excess generation of ROS may result in cell death or different pathological processes. The study also highlights the complex nature of malnutrition injury in which ROS correlates with the hepatic injury in a cause-and-effect manner. The male offspring with intrauterine growth restriction (IUGR) caused by the isocaloric low-protein diet (8%) showed decreased liver and body weight at birth. Hepatic cholesterol levels and serum transaminase increase, at weaning (24 day of age). We observed excess generation of ROS, carbonyl group and lipoperoxidation with that may result in cell death or different pathological processes in the liver. Conclusion: This study would suggests that liver injury due to accelerated release of toxic oxygen species and impaired antioxidant status may contribute to the high susceptibility to suffer metabolic diseases, that are related to diet in early life and that manifest in adulthood.
Highlights
Intrauterine growth restriction (IUGR) affects 3–10% of pregnancies, and is recognized as the leading cause of intrauterine fetal death and the second leading cause of neonatal Death [1, 2]
This study would suggests that liver injury due to accelerated release of toxic oxygen species and impaired antioxidant status may contribute to the high susceptibility to suffer metabolic diseases, that are related to diet in early life and that manifest in adulthood
Studies of animal models are consistent with the concept that adverse events in utero predispose the offspring toward the later development of metabolic Syndrome [11]
Summary
Intrauterine growth restriction (IUGR) affects 3–10% of pregnancies, and is recognized as the leading cause of intrauterine fetal death and the second leading cause of neonatal Death [1, 2]. Numerous epidemiological studies have demonstrated a strong association between low birth weight and subsequent development of metabolic syndrome, consisting of type 2 diabetes mellitus, obesity, dyslipidaemia, hypertension and coronary artery disease [3,4,5,6,7,8,9] These findings led to the “fetal origins of adult disease hypothesis”, which is described as the developmental origins of health and disease hypothesis [10]. Studies of animal models are consistent with the concept that adverse events in utero predispose the offspring toward the later development of metabolic Syndrome [11] All these data suggested that the underlying causes of the metabolic syndrome in humans are complicated and controversial, maternal undernutrition may be a causal factorFetal intrauterine growth restriction (IUGR) occurs in humans as a consequence of poor maternal nutrition.
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