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Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice
Several studies have suggested that signals emerging from white adipose tissue can contribute to the control of longevity. In turn, aging is associated with perturbed regulation and partitioning of fat depots and insulin resistance. However, the exact mechanisms involved in these relationships remai...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944987/ https://www.ncbi.nlm.nih.gov/pubmed/29746487 http://dx.doi.org/10.1371/journal.pone.0196603 |
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author | Carter, Sophie Miard, Stéphanie Boivin, Louise Sallé-Lefort, Sandrine Picard, Frédéric |
author_facet | Carter, Sophie Miard, Stéphanie Boivin, Louise Sallé-Lefort, Sandrine Picard, Frédéric |
author_sort | Carter, Sophie |
collection | PubMed |
description | Several studies have suggested that signals emerging from white adipose tissue can contribute to the control of longevity. In turn, aging is associated with perturbed regulation and partitioning of fat depots and insulin resistance. However, the exact mechanisms involved in these relationships remain undetermined. Using RAP-PCR on adipose tissue of young and old male mice coupled with qPCR validation, we have uncovered the long non-coding RNA Malat1 as a gene robustly downregulated in visceral white adipose tissue (vWAT) during normal aging in male mice and men. Reductions in Malat1 expression in subcutaneous WAT (scWAT) were also observed in genetic (ob and db) as well as diet-induced models of obesity. Based on these findings, Malat1+/+ and Malat1-/- mouse littermates were thus probed to detect whether loss of Malat1 would impact age or diet-induced gain in fat mass and development of glucose intolerance. Contrary to this hypothesis, male and female Malat1-deficient mice gained as much weight, and developed insulin resistance to a similar extent as their Malat1+/+ littermates when studied up to eight months old on regular chow or a high-fat, high-sucrose diet. Moreover, we observed no marked difference in oxygen consumption, food intake, or lipid profiles between Malat1+/+ and Malat1-/- mice. Therefore, we conclude that the overall metabolic impact of the absence of Malat1 on adipose tissue accretion and glucose intolerance is either physiologically not relevant upon aging and obesity, or that it is masked by as yet unknown compensatory mechanisms. |
format | Online Article Text |
id | pubmed-5944987 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-59449872018-05-25 Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice Carter, Sophie Miard, Stéphanie Boivin, Louise Sallé-Lefort, Sandrine Picard, Frédéric PLoS One Research Article Several studies have suggested that signals emerging from white adipose tissue can contribute to the control of longevity. In turn, aging is associated with perturbed regulation and partitioning of fat depots and insulin resistance. However, the exact mechanisms involved in these relationships remain undetermined. Using RAP-PCR on adipose tissue of young and old male mice coupled with qPCR validation, we have uncovered the long non-coding RNA Malat1 as a gene robustly downregulated in visceral white adipose tissue (vWAT) during normal aging in male mice and men. Reductions in Malat1 expression in subcutaneous WAT (scWAT) were also observed in genetic (ob and db) as well as diet-induced models of obesity. Based on these findings, Malat1+/+ and Malat1-/- mouse littermates were thus probed to detect whether loss of Malat1 would impact age or diet-induced gain in fat mass and development of glucose intolerance. Contrary to this hypothesis, male and female Malat1-deficient mice gained as much weight, and developed insulin resistance to a similar extent as their Malat1+/+ littermates when studied up to eight months old on regular chow or a high-fat, high-sucrose diet. Moreover, we observed no marked difference in oxygen consumption, food intake, or lipid profiles between Malat1+/+ and Malat1-/- mice. Therefore, we conclude that the overall metabolic impact of the absence of Malat1 on adipose tissue accretion and glucose intolerance is either physiologically not relevant upon aging and obesity, or that it is masked by as yet unknown compensatory mechanisms. Public Library of Science 2018-05-10 /pmc/articles/PMC5944987/ /pubmed/29746487 http://dx.doi.org/10.1371/journal.pone.0196603 Text en © 2018 Carter et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Carter, Sophie Miard, Stéphanie Boivin, Louise Sallé-Lefort, Sandrine Picard, Frédéric Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
title | Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
title_full | Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
title_fullStr | Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
title_full_unstemmed | Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
title_short | Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
title_sort | loss of malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944987/ https://www.ncbi.nlm.nih.gov/pubmed/29746487 http://dx.doi.org/10.1371/journal.pone.0196603 |
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