Cardiometabolic Effects of Postnatal High-Fat Diet Consumption in Offspring Exposed to Maternal Protein Restriction In Utero.

In recent decades, the high incidence of infectious and parasitic diseases has been replaced by a high prevalence of chronic and degenerative diseases. Concomitantly, there have been profound changes in the behavior and eating habits of families around the world, characterizing a "nutritional transition" phenomenon, which refers to a shift in diet in response to modernization, urbanization, or economic development from undernutrition to the excessive consumption of hypercaloric and ultra-processed foods. Protein malnutrition that was a health problem in the first half of the 20th century has now been replaced by high-fat diets, especially diets high in saturated fat, predisposing consumers to overweight and obesity. This panorama points us to the alarming coexistence of both malnutrition and obesity in the same population. In this way, individuals whose mothers were undernourished early in pregnancy and then exposed to postnatal hyperlipidic nutrition have increased risk factors for developing metabolic dysfunction and cardiovascular diseases in adulthood. Thus, our major aim was to review the cardiometabolic effects resulting from postnatal hyperlipidic diets in protein-restricted subjects, as well as to examine the epigenetic repercussions occasioned by the nutritional transition.

Does the enriched environment alter memory capacity in malnourished rats by modulating BDNF expression?

Environmental factors interfere in the neural plasticity processes. Among these, malnutrition in the early stages of life stands out as one of the main non-genetic factors that can interfere in the morphofunctional development of the nervous system. Furthermore, sensory stimulation from enriched environments (EE) also interferes with neural development. These two factors can modify areas related to memory and learning as the hippocampus, through mechanisms related to the gene expression of brain-derived neurotrophic factor (BDNF). The BDNF may interfere in synaptic plasticity processes, such as memory. In addition, these changes in early life may affect the functioning of the hippocampus during adulthood through mechanisms mediated by BDNF. Therefore, this study aims to conduct a literature review on the effects of early malnutrition on memory and the relationship between the underlying mechanisms of EE, BDNF gene expression, and memory. In addition, there are studies that demonstrate the effect of EE reversal on exposure to changes in the functioning of hippocampal malnutrition in adult rats that were prematurely malnourished. Thereby, evidence from the scientific literature suggests that the mechanisms of synaptic plasticity in the hippocampus of adult animals are influenced by malnutrition and EE, and these alterations may involve the participation of BDNF as a key regulator in memory processes in the adult animal hippocampus.

Effects of maternal low-protein diet and spontaneous physical activity on the transcription of neurotrophic factors in the placenta and the brains of mothers and offspring rats.

Maternal protein restriction and physical activity can affect the interaction mother-placenta-fetus. This study quantified the gene expression of brain-derived neurotrophic factor (BDNF), neurothrophin 4, tyrosine kinase receptor B (TrkB/NTRK2), insulin-like growth factor (IGF-1), and insulin-like growth factor receptor (IGF-1r) in the different areas of mother's brain (hypothalamus, hippocampus, and cortex), placenta, and fetus' brain of rats. Female Wistar rats (n = 20) were housed in cages containing a running wheel for 4 weeks before gestation. According to the distance spontaneously traveled daily, rats were classified as inactive or active. During gestation, on continued access to the running wheel, active and inactive groups were randomized to receive normoprotein diet (18% protein) or a low-protein (LP) diet (8% protein). At day 20 of gestation, gene expression of neurotrophic factors was analyzed by quantitative polymerase chain reaction in different brain areas and the placenta. Dams submitted to a LP diet during gestation showed upregulation of IGF-1r and BDNF messenger RNA in the hypothalamus, IGF-1r and NTRK2 in the hippocampus, and BDNF, NTRK2, IGF-1 and IGF-1r in the cortex. In the placenta, there was a downregulation of IGF-1. In the brain of pups from mothers on LP diet, IGF-1r and NTRK2 were downregulated. Voluntary physical activity attenuated the effects of LP diet on IGF-1r in the hypothalamus, IGF-1r and NTRK2 in the hippocampus, IGF-1 in the placenta, and NTRK2 in the fetus' brain. In conclusion, both maternal protein restriction and spontaneous physical activity influence the gene expression of BDNF, NTRK2, IGF-1, and IGF-1r, with spontaneous physical activity being able to normalize in part the defects caused by protein restriction during pregnancy.