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Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood

Excess dietary fructose intake is a major public health concern due to its deleterious effect to cause various metabolic and cardiovascular diseases. However, little is known about the effects of high-fructose consumption during pregnancy on offspring metabolic health in adulthood. Here, we show tha...

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Autores principales: Wang, Peng, Wu, Tian, Fu, Qinghua, Liao, Qichao, Li, Yan, Huang, Tengda, Li, Yixing, Zhou, Lei, Song, Ziyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9036479/
https://www.ncbi.nlm.nih.gov/pubmed/35479745
http://dx.doi.org/10.3389/fnut.2022.848983
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author Wang, Peng
Wu, Tian
Fu, Qinghua
Liao, Qichao
Li, Yan
Huang, Tengda
Li, Yixing
Zhou, Lei
Song, Ziyi
author_facet Wang, Peng
Wu, Tian
Fu, Qinghua
Liao, Qichao
Li, Yan
Huang, Tengda
Li, Yixing
Zhou, Lei
Song, Ziyi
author_sort Wang, Peng
collection PubMed
description Excess dietary fructose intake is a major public health concern due to its deleterious effect to cause various metabolic and cardiovascular diseases. However, little is known about the effects of high-fructose consumption during pregnancy on offspring metabolic health in adulthood. Here, we show that maternal consumption of 20% (w/v) fructose water during pregnancy does not alter the metabolic balance of offspring with a chow diet, but predisposes them to obesity, fatty liver, and insulin resistance when challenged by a high-fat diet. Mechanistically, diet-induced brown fat reprogramming and global energy expenditure in offspring of fructose-fed dams are impaired. RNA-seq analysis of the fetal brown fat tissue reveals that the myogenic pathway is predominantly upregulated in the fructose-treated group. Meanwhile, circulating fructose level is found to be significantly elevated in both fructose-fed dams and their fetuses. Importantly fructose gavage also acutely activates the myogenic program in mice brown fat. Together, our data suggest that maternal high-fructose intake impairs fetal brown fat development, resultantly attenuates diet-induced thermogenesis and causes metabolic disorders in adult offspring probably through inducing myogenic signature in brown fat at the fetal stage.
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spelling pubmed-90364792022-04-26 Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood Wang, Peng Wu, Tian Fu, Qinghua Liao, Qichao Li, Yan Huang, Tengda Li, Yixing Zhou, Lei Song, Ziyi Front Nutr Nutrition Excess dietary fructose intake is a major public health concern due to its deleterious effect to cause various metabolic and cardiovascular diseases. However, little is known about the effects of high-fructose consumption during pregnancy on offspring metabolic health in adulthood. Here, we show that maternal consumption of 20% (w/v) fructose water during pregnancy does not alter the metabolic balance of offspring with a chow diet, but predisposes them to obesity, fatty liver, and insulin resistance when challenged by a high-fat diet. Mechanistically, diet-induced brown fat reprogramming and global energy expenditure in offspring of fructose-fed dams are impaired. RNA-seq analysis of the fetal brown fat tissue reveals that the myogenic pathway is predominantly upregulated in the fructose-treated group. Meanwhile, circulating fructose level is found to be significantly elevated in both fructose-fed dams and their fetuses. Importantly fructose gavage also acutely activates the myogenic program in mice brown fat. Together, our data suggest that maternal high-fructose intake impairs fetal brown fat development, resultantly attenuates diet-induced thermogenesis and causes metabolic disorders in adult offspring probably through inducing myogenic signature in brown fat at the fetal stage. Frontiers Media S.A. 2022-04-11 /pmc/articles/PMC9036479/ /pubmed/35479745 http://dx.doi.org/10.3389/fnut.2022.848983 Text en Copyright © 2022 Wang, Wu, Fu, Liao, Li, Huang, Li, Zhou and Song. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other 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 accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Nutrition
Wang, Peng
Wu, Tian
Fu, Qinghua
Liao, Qichao
Li, Yan
Huang, Tengda
Li, Yixing
Zhou, Lei
Song, Ziyi
Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood
title Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood
title_full Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood
title_fullStr Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood
title_full_unstemmed Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood
title_short Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood
title_sort maternal high-fructose intake activates myogenic program in fetal brown fat and predisposes offspring to diet-induced metabolic dysfunctions in adulthood
topic Nutrition
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9036479/
https://www.ncbi.nlm.nih.gov/pubmed/35479745
http://dx.doi.org/10.3389/fnut.2022.848983
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