Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice

Abstract Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offspring energy homeostasis in rodents. 17β-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER) α. Therefore, we hypothesized that females lacking ERα would be more su...

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Autores principales:	Troy A. Roepke, Ali Yasrebi, Alejandra Villalobos, Elizabeth A. Krumm, Jennifer A. Yang, Kyle J. Mamounis
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5d584998040a4876b65ce071130d2172
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spelling	oai:doaj.org-article:5d584998040a4876b65ce071130d21722021-12-02T15:06:20ZLoss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice10.1038/s41598-017-06560-x2045-2322https://doaj.org/article/5d584998040a4876b65ce071130d21722017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06560-xhttps://doaj.org/toc/2045-2322Abstract Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offspring energy homeostasis in rodents. 17β-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER) α. Therefore, we hypothesized that females lacking ERα would be more susceptible to maternal HFD. To address this question, heterozygous ERα knockout (WT/KO) dams were fed a control breeder chow diet (25% fat) or a semi-purified HFD (45% fat) 4 weeks prior to mating with WT/KO males or heterozygous males with an ERα DNA-binding domain mutation knocked in (WT/KI) to produce WT, ERα KO, or ERα KIKO females lacking ERE-dependent ERα signaling. Maternal HFD increased body weight in WT and KIKO, in part, due to increased adiposity and daytime carbohydrate utilization in WT and KIKO, while increasing nighttime fat utilization in KO. Maternal HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression of Kiss1 and Esr1 (ERα) and liver expression of G6pc and Pepck in WT and KIKO. Contrary to our hypothesis, these data suggest that loss of ERα signaling blocks the influence of maternal HFD on energy homeostasis, inflammation, and hypothalamic and liver gene expression and that restoration of ERE-independent ERα signaling partially reestablishes susceptibility to maternal HFD.Troy A. RoepkeAli YasrebiAlejandra VillalobosElizabeth A. KrummJennifer A. YangKyle J. MamounisNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Troy A. Roepke Ali Yasrebi Alejandra Villalobos Elizabeth A. Krumm Jennifer A. Yang Kyle J. Mamounis Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
description	Abstract Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offspring energy homeostasis in rodents. 17β-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER) α. Therefore, we hypothesized that females lacking ERα would be more susceptible to maternal HFD. To address this question, heterozygous ERα knockout (WT/KO) dams were fed a control breeder chow diet (25% fat) or a semi-purified HFD (45% fat) 4 weeks prior to mating with WT/KO males or heterozygous males with an ERα DNA-binding domain mutation knocked in (WT/KI) to produce WT, ERα KO, or ERα KIKO females lacking ERE-dependent ERα signaling. Maternal HFD increased body weight in WT and KIKO, in part, due to increased adiposity and daytime carbohydrate utilization in WT and KIKO, while increasing nighttime fat utilization in KO. Maternal HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression of Kiss1 and Esr1 (ERα) and liver expression of G6pc and Pepck in WT and KIKO. Contrary to our hypothesis, these data suggest that loss of ERα signaling blocks the influence of maternal HFD on energy homeostasis, inflammation, and hypothalamic and liver gene expression and that restoration of ERE-independent ERα signaling partially reestablishes susceptibility to maternal HFD.
format	article
author	Troy A. Roepke Ali Yasrebi Alejandra Villalobos Elizabeth A. Krumm Jennifer A. Yang Kyle J. Mamounis
author_facet	Troy A. Roepke Ali Yasrebi Alejandra Villalobos Elizabeth A. Krumm Jennifer A. Yang Kyle J. Mamounis
author_sort	Troy A. Roepke
title	Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
title_short	Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
title_full	Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
title_fullStr	Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
title_full_unstemmed	Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
title_sort	loss of erα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/5d584998040a4876b65ce071130d2172
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Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice

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