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Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood

The perinatal environment plays an important role in programming many aspects of physiology and behavior including metabolism, body weight set point, energy balance regulation and predisposition to mental health-related disorders such as anxiety, depression and attention deficit hyperactivity disord...

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Autores principales: Sullivan, Elinor L., Smith, M. Susan, Grove, Kevin L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: S. Karger AG 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700139/
https://www.ncbi.nlm.nih.gov/pubmed/21079387
http://dx.doi.org/10.1159/000322038
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author Sullivan, Elinor L.
Smith, M. Susan
Grove, Kevin L.
author_facet Sullivan, Elinor L.
Smith, M. Susan
Grove, Kevin L.
author_sort Sullivan, Elinor L.
collection PubMed
description The perinatal environment plays an important role in programming many aspects of physiology and behavior including metabolism, body weight set point, energy balance regulation and predisposition to mental health-related disorders such as anxiety, depression and attention deficit hyperactivity disorder. Maternal health and nutritional status heavily influence the early environment and have a long-term impact on critical central pathways, including the melanocortinergic, serotonergic system and dopaminergic systems. Evidence from a variety of animal models including rodents and nonhuman primates indicates that exposure to maternal high-fat diet (HFD) consumption programs offspring for increased risk of adult obesity. Hyperphagia and increased preference for fatty and sugary foods are implicated as mechanisms for the increased obesity risk. The effects of maternal HFD consumption on energy expenditure are unclear, and future studies need to address the impact of perinatal HFD exposure on this important component of energy balance regulation. Recent evidence from animal models also indicates that maternal HFD consumption increases the risk of offspring developing mental health-related disorders such as anxiety. Potential mechanisms for perinatal HFD programming of neural pathways include circulating factors, such as hormones (leptin, insulin), nutrients (fatty acids, triglycerides and glucose) and inflammatory cytokines. As maternal HFD consumption and obesity are common and rapidly increasing, we speculate that future generations will be at increased risk for both metabolic and mental health disorders. Thus, it is critical that future studies identify therapeutic strategies that are effective at preventing maternal HFD-induced malprogramming.
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spelling pubmed-37001392013-07-11 Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood Sullivan, Elinor L. Smith, M. Susan Grove, Kevin L. Neuroendocrinology At the Cutting Edge The perinatal environment plays an important role in programming many aspects of physiology and behavior including metabolism, body weight set point, energy balance regulation and predisposition to mental health-related disorders such as anxiety, depression and attention deficit hyperactivity disorder. Maternal health and nutritional status heavily influence the early environment and have a long-term impact on critical central pathways, including the melanocortinergic, serotonergic system and dopaminergic systems. Evidence from a variety of animal models including rodents and nonhuman primates indicates that exposure to maternal high-fat diet (HFD) consumption programs offspring for increased risk of adult obesity. Hyperphagia and increased preference for fatty and sugary foods are implicated as mechanisms for the increased obesity risk. The effects of maternal HFD consumption on energy expenditure are unclear, and future studies need to address the impact of perinatal HFD exposure on this important component of energy balance regulation. Recent evidence from animal models also indicates that maternal HFD consumption increases the risk of offspring developing mental health-related disorders such as anxiety. Potential mechanisms for perinatal HFD programming of neural pathways include circulating factors, such as hormones (leptin, insulin), nutrients (fatty acids, triglycerides and glucose) and inflammatory cytokines. As maternal HFD consumption and obesity are common and rapidly increasing, we speculate that future generations will be at increased risk for both metabolic and mental health disorders. Thus, it is critical that future studies identify therapeutic strategies that are effective at preventing maternal HFD-induced malprogramming. S. Karger AG 2011-02 2010-11-13 /pmc/articles/PMC3700139/ /pubmed/21079387 http://dx.doi.org/10.1159/000322038 Text en Copyright © 2010 by S. Karger AG, Basel http://www.karger.com/Authors_Choice This is an open access article distributed under the terms of Karger's Author's Choice™ licensing agreement, adapted from the Creative Commons Attribution Non-Commercial 2.5 license. This license allows authors to re-use their articles for educational and research purposes as long as the author and the journal are fully acknowledged.
spellingShingle At the Cutting Edge
Sullivan, Elinor L.
Smith, M. Susan
Grove, Kevin L.
Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood
title Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood
title_full Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood
title_fullStr Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood
title_full_unstemmed Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood
title_short Perinatal Exposure to High-Fat Diet Programs Energy Balance, Metabolism and Behavior in Adulthood
title_sort perinatal exposure to high-fat diet programs energy balance, metabolism and behavior in adulthood
topic At the Cutting Edge
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700139/
https://www.ncbi.nlm.nih.gov/pubmed/21079387
http://dx.doi.org/10.1159/000322038
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