Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo
Abstract Tumor protein 53‐induced nuclear protein 1 (TP53INP1) deficiency leads to oxidative stress‐associated obesity and insulin resistance. Although skeletal muscle has a predominant role in the development of metabolic syndrome, the bioenergetics and functional consequences of TP53INP1 deficienc...
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doaj-d2c703cbe2a94a63a89de256a78ffcf32020-11-25T03:05:33ZengWileyPhysiological Reports2051-817X2019-05-01710n/an/a10.14814/phy2.14055Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivoJulie Warnez‐Soulie0Michael Macia1Sophie Lac2Emilie Pecchi3Monique Bernard4David Bendahan5Marc Bartoli6Alice Carrier7Benoît Giannesini8Aix Marseille Univ, INSERM, MMG Marseille FranceAix Marseille Univ, CNRS, CRMBM Marseille FranceAix Marseille Univ, CNRS, INSERM, Institut Paoli‐Calmettes, CRCM Marseille FranceAix Marseille Univ, CNRS, CRMBM Marseille FranceAix Marseille Univ, CNRS, CRMBM Marseille FranceAix Marseille Univ, CNRS, CRMBM Marseille FranceAix Marseille Univ, INSERM, MMG Marseille FranceAix Marseille Univ, CNRS, INSERM, Institut Paoli‐Calmettes, CRCM Marseille FranceAix Marseille Univ, CNRS, CRMBM Marseille FranceAbstract Tumor protein 53‐induced nuclear protein 1 (TP53INP1) deficiency leads to oxidative stress‐associated obesity and insulin resistance. Although skeletal muscle has a predominant role in the development of metabolic syndrome, the bioenergetics and functional consequences of TP53INP1 deficiency upon this tissue remain undocumented. To clarify this issue, gastrocnemius muscle mechanical performance, energy metabolism, and anatomy were investigated in TP53INP1‐deficient and wild‐type mice using a multidisciplinary approach implementing noninvasive multimodal‐NMR techniques. TP53INP1 deficiency increased body adiposity but did not affect cytosolic oxidative stress, lipid content, and mitochondrial pool and capacity in myocyte. During a fatiguing bout of exercise, the in vivo oxidative ATP synthesis capacity was dramatically reduced in TP53INP1‐deficient mice despite ADP level (the main in vivo stimulator of mitochondrial respiration) did not differ between both genotypes. Moreover, TP53INP1 deficiency did not alter fatigue resistance but paradoxically increased the contractile force, whereas there were no differences for muscle fiber‐type distribution and calcium homeostasis between both genotypes. In addition, muscle proton efflux was decreased in TP53INP1‐deficient mice, thereby indicating a reduced blood supply. In conclusion, TP53INP1 plays a role in muscle function and bioenergetics through oxidative capacity impairment possibly as the consequence of abnormal mitochondrial respiration regulation and/or defective blood supply.https://doi.org/10.14814/phy2.14055Insulin resistancemitochondrial functionmultimodal NMRobesityoxidative stress |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Julie Warnez‐Soulie Michael Macia Sophie Lac Emilie Pecchi Monique Bernard David Bendahan Marc Bartoli Alice Carrier Benoît Giannesini |
spellingShingle |
Julie Warnez‐Soulie Michael Macia Sophie Lac Emilie Pecchi Monique Bernard David Bendahan Marc Bartoli Alice Carrier Benoît Giannesini Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo Physiological Reports Insulin resistance mitochondrial function multimodal NMR obesity oxidative stress |
author_facet |
Julie Warnez‐Soulie Michael Macia Sophie Lac Emilie Pecchi Monique Bernard David Bendahan Marc Bartoli Alice Carrier Benoît Giannesini |
author_sort |
Julie Warnez‐Soulie |
title |
Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo |
title_short |
Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo |
title_full |
Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo |
title_fullStr |
Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo |
title_full_unstemmed |
Tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo |
title_sort |
tumor protein 53‐induced nuclear protein 1 deficiency alters mouse gastrocnemius muscle function and bioenergetics in vivo |
publisher |
Wiley |
series |
Physiological Reports |
issn |
2051-817X |
publishDate |
2019-05-01 |
description |
Abstract Tumor protein 53‐induced nuclear protein 1 (TP53INP1) deficiency leads to oxidative stress‐associated obesity and insulin resistance. Although skeletal muscle has a predominant role in the development of metabolic syndrome, the bioenergetics and functional consequences of TP53INP1 deficiency upon this tissue remain undocumented. To clarify this issue, gastrocnemius muscle mechanical performance, energy metabolism, and anatomy were investigated in TP53INP1‐deficient and wild‐type mice using a multidisciplinary approach implementing noninvasive multimodal‐NMR techniques. TP53INP1 deficiency increased body adiposity but did not affect cytosolic oxidative stress, lipid content, and mitochondrial pool and capacity in myocyte. During a fatiguing bout of exercise, the in vivo oxidative ATP synthesis capacity was dramatically reduced in TP53INP1‐deficient mice despite ADP level (the main in vivo stimulator of mitochondrial respiration) did not differ between both genotypes. Moreover, TP53INP1 deficiency did not alter fatigue resistance but paradoxically increased the contractile force, whereas there were no differences for muscle fiber‐type distribution and calcium homeostasis between both genotypes. In addition, muscle proton efflux was decreased in TP53INP1‐deficient mice, thereby indicating a reduced blood supply. In conclusion, TP53INP1 plays a role in muscle function and bioenergetics through oxidative capacity impairment possibly as the consequence of abnormal mitochondrial respiration regulation and/or defective blood supply. |
topic |
Insulin resistance mitochondrial function multimodal NMR obesity oxidative stress |
url |
https://doi.org/10.14814/phy2.14055 |
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