Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution

Abstract This study explores if unhealthy lipoprotein distribution (LPD) impairs the anabolic and amino acid sensing responses to whey-protein feeding. Thus, if impairment of such anabolic response to protein consumption is seen by the LPD this may negatively affect the skeletal muscle mass. Muscle...

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Autores principales:	Jakob Agergaard, Mie Cecilie Faber Zillmer, Josué L. Castro-Mejía, Kenneth Mertz, Witold Kot, Grith Højfeldt, Gerrit van Hall, Dennis S. Nielsen, Peter Schjerling, Lars Holm
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a6c45fb3112845e6ad3da6e163c13379
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spelling	oai:doaj.org-article:a6c45fb3112845e6ad3da6e163c133792021-12-02T18:50:59ZImpaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution10.1038/s41598-021-96000-82045-2322https://doaj.org/article/a6c45fb3112845e6ad3da6e163c133792021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-96000-8https://doaj.org/toc/2045-2322Abstract This study explores if unhealthy lipoprotein distribution (LPD) impairs the anabolic and amino acid sensing responses to whey-protein feeding. Thus, if impairment of such anabolic response to protein consumption is seen by the LPD this may negatively affect the skeletal muscle mass. Muscle protein synthesis (MPS) was measured by puromycin labeling in Apolipoprotein E knockout (Apoe KO), characterized by an unhealthy LPD, and wild type mice post-absorptive at 10 and 20 weeks, and post-prandial after whey-protein feeding at 20 weeks. Hypertrophy signaling and amino acid sensing mechanisms were studied and gut microbiome diversity explored. Surprisingly, whey-protein feeding did not affect MPS. p-mTOR and p-4E-BP1 was increased 2 h after whey-protein feeding in both genotypes, but with general lower levels in Apoe KO compared to wild type. At 20 weeks of age, Apoe KO had a greater mRNA-expression for SNAT2, CD98, ATF4 and GCN2 compared to wild type. These responses were not associated with gut microbiota compositional differences. Regardless of LPD status, MPS was similar in Apoe KO and wild type. Surprisingly, whey-protein did not stimulate MPS. However, Apoe KO had lower levels of hypertrophy signaling, was amino acid deprived, and had impaired amino acid sensing mechanisms.Jakob AgergaardMie Cecilie Faber ZillmerJosué L. Castro-MejíaKenneth MertzWitold KotGrith HøjfeldtGerrit van HallDennis S. NielsenPeter SchjerlingLars HolmNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jakob Agergaard Mie Cecilie Faber Zillmer Josué L. Castro-Mejía Kenneth Mertz Witold Kot Grith Højfeldt Gerrit van Hall Dennis S. Nielsen Peter Schjerling Lars Holm Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution
description	Abstract This study explores if unhealthy lipoprotein distribution (LPD) impairs the anabolic and amino acid sensing responses to whey-protein feeding. Thus, if impairment of such anabolic response to protein consumption is seen by the LPD this may negatively affect the skeletal muscle mass. Muscle protein synthesis (MPS) was measured by puromycin labeling in Apolipoprotein E knockout (Apoe KO), characterized by an unhealthy LPD, and wild type mice post-absorptive at 10 and 20 weeks, and post-prandial after whey-protein feeding at 20 weeks. Hypertrophy signaling and amino acid sensing mechanisms were studied and gut microbiome diversity explored. Surprisingly, whey-protein feeding did not affect MPS. p-mTOR and p-4E-BP1 was increased 2 h after whey-protein feeding in both genotypes, but with general lower levels in Apoe KO compared to wild type. At 20 weeks of age, Apoe KO had a greater mRNA-expression for SNAT2, CD98, ATF4 and GCN2 compared to wild type. These responses were not associated with gut microbiota compositional differences. Regardless of LPD status, MPS was similar in Apoe KO and wild type. Surprisingly, whey-protein did not stimulate MPS. However, Apoe KO had lower levels of hypertrophy signaling, was amino acid deprived, and had impaired amino acid sensing mechanisms.
format	article
author	Jakob Agergaard Mie Cecilie Faber Zillmer Josué L. Castro-Mejía Kenneth Mertz Witold Kot Grith Højfeldt Gerrit van Hall Dennis S. Nielsen Peter Schjerling Lars Holm
author_facet	Jakob Agergaard Mie Cecilie Faber Zillmer Josué L. Castro-Mejía Kenneth Mertz Witold Kot Grith Højfeldt Gerrit van Hall Dennis S. Nielsen Peter Schjerling Lars Holm
author_sort	Jakob Agergaard
title	Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution
title_short	Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution
title_full	Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution
title_fullStr	Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution
title_full_unstemmed	Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution
title_sort	impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in apoe knockout mice with an unhealthy lipoprotein distribution
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a6c45fb3112845e6ad3da6e163c13379
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Impaired skeletal muscle hypertrophy signaling and amino acid deprivation response in Apoe knockout mice with an unhealthy lipoprotein distribution

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