Editorial on the Research Topic.
Obesogenic Environmental Conditions Affect Neurodevelopment and Neurodegeneratio

Bravo, Javier A.

Figueroa, Johnny Davis

Guzmán-Ramos, Kioko Rubí

Krügel, Ute

Pacheco-López, Gustavo

Pérez-Morales, Marcel

English

Qucosa - Publikationsserver der Universität Leipzig

EDITORIALpublished: 04 August 2021doi: 10.3389/fnins.2021.724503Frontiers in Neuroscience | www.frontiersin.org 1 August 2021 | Volume 15 | Article 724503Edited and reviewed by:Jong-Min Kim,Seoul National University BundangHospital, South Korea*Correspondence:Gustavo Pacheco-Lópezg.pacheco@correo.ler.uam.mxMarcel Pérez-Moralesm.perez@correo.ler.uam.mxSpecialty section:This article was submitted toNeuroenergetics, Nutrition and BrainHealth,a section of the journalFrontiers in NeuroscienceReceived: 13 June 2021Accepted: 09 July 2021Published: 04 August 2021Citation:Pacheco-López G, Pérez-Morales M,Guzmán-Ramos KR, Figueroa JD,Krügel U and Bravo JA (2021)Editorial: Obesogenic EnvironmentalConditions Affect Neurodevelopmentand Neurodegeneration.Front. Neurosci. 15:724503.doi: 10.3389/fnins.2021.724503Editorial: Obesogenic EnvironmentalConditions Affect Neurodevelopmentand NeurodegenerationGustavo Pacheco-López 1*, Marcel Pérez-Morales 1*, Kioko Rubí Guzmán-Ramos 1,Johnny Davis Figueroa 2, Ute Krügel 3 and Javier A. Bravo 41Health Sciences Department, Metropolitan Autonomous University (UAM), Campus Lerma, Lerma, Mexico, 2 School ofMedicine, Loma Linda University, Loma Linda, CA, United States, 3Medical Faculty, Leipzig University, Leipzig, Germany,4 Pontificia Universidad Católica de Valparaiso, Valparaiso, ChileKeywords: obesogenic environments, neurodevelopmental diseases, neurodegenerative diseases, obesity,energy homeostasisEditorial on the Research TopicObesogenic Environmental Conditions Affect Neurodevelopment and NeurodegenerationThe classical debate between nativism (nature, genes) and empiricism (environment, nurture)originated in ancient Greece and developed in the Renaissance, including analogies of Aristotleand metaphors of Gottfried Wilhelm Leibniz about the contents of the mind, persists to ourdays in neurobiology. The subject of this Research Topic is an example of this controversy.From a methodological perspective, an obesogenic environment is an experimental approachin which environmental manipulations, such as exposure to hypercaloric diets, drinking sugar-sweetened beverages (i.e., diet-induced obesity), and reduced physical activity, separately or incombination, may lead to metabolic imbalances, weight gain, and finally to adiposity. The scientificfield continues making strides to determine the contribution of the myriad of obesogenic factorsmodulating energy homeostasis.In this Research Topic, six original papers, two reviews, and one mini-review summarize theimpact of several obesogenic factors upon food intake regulation, obesity-associated biomarkers,and describe several behavioral and molecular approaches that enhance our understanding ofobesity. In the context of the sedentary lifestyle and the constant availability of junk foodthat has dramatically increased in the last 30 years all over the world, Flores-Dorantes et al.provide an integrative view on the relationship between obesogenic environments and obesity,with both neurodegenerative and neurodevelopmental diseases. The authors emphasize theinvolvement of genes traditionally associated with food intake regulation, such as those thatcode for the leptin-melanocortin pathway proteins and their incidence on neurodegenerative andneurodevelopmental diseases. They call our attention to the gene-environment interaction thatpromotes an imbalance between caloric intake and energy expenditure. They provide furtherevidence for common neurobiological pathways between obesity and neurodegenerative diseases,suggesting that metabolic syndrome and obesity are risk factors for Parkinson’s disease andAlzheimer’s disease (AD).Whereas a relationship between obesity and the development of neurodegenerative diseasesis widely accepted, we are just beginning to understand how environmental factors and themicrobiome contribute to these conditions. Bello-Medina et al. demonstrate evidence for spatialmemory deficits, differences in beta diversity, and lower relative abundances of Actinobacteria andTM7 in the gut microbiota of 3 months-old 3xTg-ADmice, one of the most used transgenic modelsof AD, compared to non-transgenic mice. Their results suggest that microbiota alterations could bePacheco-López et al. Editorial: Obesogenic Environment Affects Brain Homeostasisrelated causally to cognitive decline and may be employed asnon-invasive biomarkers of AD, even at a presymptomatic stage.Peleg-Raibstein focuses on the impact of maternalovernutrition by highly palatable diets, high-fat diets, acombination of high-fat-high-sugar diets, or cafeteria diets onthe development of obesity and cardio-metabolic dysfunctionand cognitive aging in the progeny. The article emphasizes therisk of unhealthy food environments provided by parents andthe consequent exposure of their children. The author points todifficulties to discern between genetic and environmental riskfactors to develop obesity and brain pathologies in the offspring.Related to these concepts, Cruz-Carrillo et al. employed a 9-weekmaternal overnutrition protocol. The authors report that theoffspring from cafeteria diet-fed mothers exhibit an increasedmotivation to obtain pellets in operant tasks and reinforce theirorexigenic response following subcutaneous injection of ghrelin.This behavior was associated with a higher global methylationin the shell region of the nucleus accumbens (NAcSh) andcorrelated with changes in the expression of pro-inflammatorycytokines. These results propose that high caloric nutritionalintake during pregnancy and lactation increases the susceptibilityto develop addictive-like behavior patterns in the progeny.Apart from influencing obesity and metabolic dysfunction,Tsan et al. review literature in which overconsumption ofhighly palatable and dense foods leads to long-lasting multipleneurocognitive impairments in diverse rodent models. Theyconclude that overconsumption of Western diets during criticalneurodevelopment stages is associated with detrimental cognitiveperformance across the lifespan. An example of this intricatedrelationship is given by Vega-Torres et al. In their study,the consumption of a Western-like high-saturated diet byadolescent rats for only 1 week is sufficient to impair emotionalreactivity and anxiety. Cued fear extinction memory andneuronal activation of the basomedial amygdala attenuated, andcorticosterone mRNA levels in the medial prefrontal cortexincreased, altogether reveal the harmful impact of short-termexposure to obesogenic environments on the corticolimbiccircuitry and emotional regulation during specific stages ofneurodevelopment. Another study provided by Han et al.investigated the effect of a much more chronic exposure ofyoung C57BL/6J mice to a high-fat diet. In their study, bodyweight, anxiety-like behavior, and, at the molecular level, themidbrain content of dopamine and D2 dopamine receptorsincreased after chronic diet exposure. From the pharmacologicalperspective and in line with food intake-associated dopaminergicactivity, Kalyanasundar et al. evaluated the effect of D-norpseudoephedrine (NPE, also Cathine), an amphetamine-like sympathomimetic and anorexigenic drug, on food intake,body weight loss, and locomotion. Their results suggestthat NPE-induced anorexia and body weight loss modulatesneuronal spiking activity in the NAcSh. Though NPE is anAfrican lifestyle drug with addiction risk, as an experimentaltool, it elucidates feeding regulation associated with NAcShneurons’ activity in part controlled by midbrain dopaminergicneurons. Regarding the genetic aspects of metabolic diseases,Amaya et al. performed a translational study in AdKO2.0transgenic mice, an animal model of Cushing’s syndrome (CS),which is characterized by hypercorticosteronemia and metabolicabnormalities predisposing for obesity and metabolic syndrome,due to an inactivation of the gene encoding the regulatorysubunit 1 alpha of the PKA, targeted to the adrenal cortex.Long-term exposure to high plasma glucocorticoids is stronglyrelated to the gain of visceral tissue and stimulation of lipogenicpathways triggered by chronic stress. Their study shows overallparallels between imaging data from CS patients and AdKO2.0transgenic mice as there is volume reduction in several brainareas and lower astrocytic and microglial markers, providing theopportunity to study the molecular basis and consequences ofhypercorticosteronemia in a preclinical model.The articles included in this Research Topic contributeto a more profound view of the complex relationship andpotential causality between various obesogenic environmentalconditions with the etiology of relevant neurodevelopmental andneurodegenerative diseases. The editors of this topic want tothank all the authors for their important contributions.AUTHOR CONTRIBUTIONSAll authors listed have made a substantial, direct and intellectualcontribution to the work, and approved it for publication.FUNDINGThis research was partially supported by Grants provided fromthe Consejo Nacional de Ciencia y Tecnología (CONACYT)-Mexico, Grants No: CB-2015 255399, DAAD-PROALMEX267761, and OBETEEN-273553 to GP-L, Universidad AutónomaMetropolitana (UAM) institutional fund to GP-L, and Grantprovided by the Deutsche Forschungsgemeinschaft (DFG) AOBJ:624810 to UK.Conflict of Interest: The authors declare that the research was conducted in theabsence of any commercial or financial relationships that could be construed as apotential conflict of interest.Publisher’s Note: All claims expressed in this article are solely those of the authorsand do not necessarily represent those of their affiliated organizations, or those ofthe publisher, the editors and the reviewers. Any product that may be evaluated inthis article, or claim that may be made by its manufacturer, is not guaranteed orendorsed by the publisher.Copyright © 2021 Pacheco-López, Pérez-Morales, Guzmán-Ramos, Figueroa, Krügeland Bravo. This is an open-access article distributed under the terms of the CreativeCommons Attribution License (CC BY). The use, distribution or reproduction inother forums is permitted, provided the original author(s) and the copyright owner(s)are credited and that the original publication in this journal is cited, in accordancewith accepted academic practice. No use, distribution or reproduction is permittedwhich does not comply with these terms.Frontiers in Neuroscience | www.frontiersin.org 2 August 2021 | Volume 15 | Article 724503

Editorial: Obesogenic Environmental Conditions Affect Neurodevelopment and Neurodegeneration

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