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Malnutrition during in utero and/or neonatal development results also in long-lasting learning deficits and a high risk of developing neurological and psychiatric disorders in later life such as depression and schizophrenia. These observations have been explained by the metabolic programming hypothesis also called nutritional programming or the developmental origins of health and disease (DOHaD). It is hypothesised that exposure to an imbalanced nutritional environment (over- or under-nutrition), during perinatal development sensitises the offspring to the development of metabolic and cognitive diseases via epigenetic changes that act during early life to program energy homeostasis and brain function. In support of this hypothesis, experimental studies in rodents have shown that the adult offspring of malnourished dams exhibit several physiological disturbances linked to the metabolic syndrome as well as impaired learning and enhanced behavioural responses to stress. However, there is no information about the cause-effect relationship between the lack of one, or several, nutrients during the critical stages of development and disease susceptibility later in life. Moreover, the molecular mechanisms affected by maternal malnutrition that underlie both the cognitive disorders and the metabolic dysfunction in the offspring remain to be identified. The overall objective of this project is to test the hypothesis that alterations in tryptophan (Trp) metabolism constitute a common causal mechanism of the cognitive and metabolic disorders induced by perinatal malnutrition. In particular, our aim is to establish a causal link between the alterations in tryptophan metabolism previously reported by the host laboratory in adult rats born to undernourished mothers and the cognitive and metabolic disorders presented by these animals.
I hold a BSc in Clinical Biochemistry from Autonomous University of San Luis Potosi, Mexico. I continued my studies towards a Master degree in Clinical Biochemistry and PhD in Biomedical Science in National Autonomous University of Mexico, Mexico City. During my PhD studies, I reinforced my conceptual and experimental expertise in the field of developmental programming, via the study of the psychiatric and cognitive disorders exhibited by the offspring of malnourished dams. I have had the opportunity to work in collaboration with Mexican and American researchers, who are leaders in the field of developmental programming, for the morphological and molecular analysis of several brain regions. I have received the SGI Thomas McDonald Travel award (2014) and FUNSALUD - Nutrition award (2014, 2016). Currently, I am a Medical Science Researcher (level “C”) in the National Institute of Nutrition”, and I belong to National research system (SNI level 1) and I study the mechanisms underlying the behavioural alterations exhibited by the offspring of obese rats.
Reyes-Castro LA, Padilla-Gómez E, Parga-Martínez NJ, Castro-Rodríguez DC, Quirarte GL, Díaz-Cintra S, Nathanielsz PW, Zambrano E., 2017. Hippocampal mechanisms in impaired spatial learning and memory in male offspring of rats fed a low-protein isocaloric diet in pregnancy and/or lactation. Hippocampus. Doi: 10.1002/ hipo.22798.
Zambrano E, Reyes-Castro LA, Nathanielsz PW, 2015. Aging, glucocorticoids and developmental programming. Age (Dordr), 37(3):9774. Doi: 10.1007/s11357-015-9774-0.
Reyes-Castro LA, Rodríguez-González GL, Chavira R, Ibáñez C, Lomas-Soria C, Rodríguez JS, Nathanielsz PW, Zambrano E., 2014. Paternal line multigenerational passage of altered risk assessment behavior in female but not male rat offspring of mothers fed a low protein diet. Physiol Behav. 140:89-95.
Reyes-Castro LA, Rodriguez JS, Charco R, Bautista CJ, Larrea F, Nathanielsz PW, Zambrano E., 2012. Maternal protein restriction in the rat during pregnancy and/or lactation alters cognitive and anxiety behaviors of female offspring. Int J Dev Neurosci; 30(1): 39-45.
Reyes-Castro LA, Rodriguez JS, Rodríguez-González GL, Chavira R, Bautista CJ, McDonald TJ, Nathanielsz PW, Zambrano E., 2012. Pre- and/or postnatal protein restriction developmentally programs affect and risk assessment behaviors in adult male rats. Behav Brain Res; 227: 324-329.