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Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice
A maternal low-protein (LP) diet during gestation and/or lactation results in metabolic syndrome in their offspring. Here, we investigated the effect of maternal LP diet during puberty and adulthood on the metabolic homeostasis of glucose and lipids in offspring. Female mice were fed with normal-pro...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9570549/ https://www.ncbi.nlm.nih.gov/pubmed/36235710 http://dx.doi.org/10.3390/nu14194057 |
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author | Huang, Xiaohua Zhuo, Yong Jiang, Dandan Zhu, Yingguo Fang, Zhengfeng Che, Lianqiang Lin, Yan Xu, Shengyu Hua, Lun Zou, Yuanfeng Huang, Chao Li, Lixia Wu, De Feng, Bin |
author_facet | Huang, Xiaohua Zhuo, Yong Jiang, Dandan Zhu, Yingguo Fang, Zhengfeng Che, Lianqiang Lin, Yan Xu, Shengyu Hua, Lun Zou, Yuanfeng Huang, Chao Li, Lixia Wu, De Feng, Bin |
author_sort | Huang, Xiaohua |
collection | PubMed |
description | A maternal low-protein (LP) diet during gestation and/or lactation results in metabolic syndrome in their offspring. Here, we investigated the effect of maternal LP diet during puberty and adulthood on the metabolic homeostasis of glucose and lipids in offspring. Female mice were fed with normal-protein (NP) diet or a LP diet for 11 weeks. Male offspring were then fed with a high-fat diet (NP-HFD and LP-HFD groups) or standard chow diet (NP-Chow and LP-Chow groups) for 4 months. Results showed that maternal LP diet during puberty and adulthood did not alter the insulin sensitivity and hepatic lipid homeostasis of their offspring under chow diet, but aggravated insulin resistance, hepatic steatosis, and hypercholesterolemia of offspring in response to a post-weaning HFD. Accordingly, transcriptomics study with offspring’s liver indicated that several genes related to glucose and lipid metabolism, including lipoprotein lipase (Lpl), long-chain acyl-CoA synthetase 1 (Acsl1), Apoprotein A1 (Apoa1), major urinary protein 19 (Mup19), cholesterol 7α hydroxylase (Cyp7a1) and fibroblast growth factor 1 (Fgf1), were changed by maternal LP diet. Taken together, maternal LP diet during puberty and adulthood could disarrange the expression of metabolic genes in the liver of offspring and aggravate insulin resistance and hepatic steatosis in offspring fed a HFD. |
format | Online Article Text |
id | pubmed-9570549 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95705492022-10-17 Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice Huang, Xiaohua Zhuo, Yong Jiang, Dandan Zhu, Yingguo Fang, Zhengfeng Che, Lianqiang Lin, Yan Xu, Shengyu Hua, Lun Zou, Yuanfeng Huang, Chao Li, Lixia Wu, De Feng, Bin Nutrients Article A maternal low-protein (LP) diet during gestation and/or lactation results in metabolic syndrome in their offspring. Here, we investigated the effect of maternal LP diet during puberty and adulthood on the metabolic homeostasis of glucose and lipids in offspring. Female mice were fed with normal-protein (NP) diet or a LP diet for 11 weeks. Male offspring were then fed with a high-fat diet (NP-HFD and LP-HFD groups) or standard chow diet (NP-Chow and LP-Chow groups) for 4 months. Results showed that maternal LP diet during puberty and adulthood did not alter the insulin sensitivity and hepatic lipid homeostasis of their offspring under chow diet, but aggravated insulin resistance, hepatic steatosis, and hypercholesterolemia of offspring in response to a post-weaning HFD. Accordingly, transcriptomics study with offspring’s liver indicated that several genes related to glucose and lipid metabolism, including lipoprotein lipase (Lpl), long-chain acyl-CoA synthetase 1 (Acsl1), Apoprotein A1 (Apoa1), major urinary protein 19 (Mup19), cholesterol 7α hydroxylase (Cyp7a1) and fibroblast growth factor 1 (Fgf1), were changed by maternal LP diet. Taken together, maternal LP diet during puberty and adulthood could disarrange the expression of metabolic genes in the liver of offspring and aggravate insulin resistance and hepatic steatosis in offspring fed a HFD. MDPI 2022-09-29 /pmc/articles/PMC9570549/ /pubmed/36235710 http://dx.doi.org/10.3390/nu14194057 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Huang, Xiaohua Zhuo, Yong Jiang, Dandan Zhu, Yingguo Fang, Zhengfeng Che, Lianqiang Lin, Yan Xu, Shengyu Hua, Lun Zou, Yuanfeng Huang, Chao Li, Lixia Wu, De Feng, Bin Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice |
title | Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice |
title_full | Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice |
title_fullStr | Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice |
title_full_unstemmed | Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice |
title_short | Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice |
title_sort | maternal low-protein diet during puberty and adulthood aggravates lipid metabolism of their offspring fed a high-fat diet in mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9570549/ https://www.ncbi.nlm.nih.gov/pubmed/36235710 http://dx.doi.org/10.3390/nu14194057 |
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