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High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue

Obesity and aging are linked to inflammation and increased risk of chronic disease. Telomeres are the endcaps of chromosomes that are regulated by telomerase, the enzyme that elongates telomeres, as well as a protein complex known as shelterin. Telomere dysfunction is associated with inflammation, a...

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Autores principales: Bloom, Samuel I., Tuluca, Andrei, Ives, Stephen J., Reynolds, Thomas H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7280005/
https://www.ncbi.nlm.nih.gov/pubmed/32512652
http://dx.doi.org/10.14814/phy2.14461
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author Bloom, Samuel I.
Tuluca, Andrei
Ives, Stephen J.
Reynolds, Thomas H.
author_facet Bloom, Samuel I.
Tuluca, Andrei
Ives, Stephen J.
Reynolds, Thomas H.
author_sort Bloom, Samuel I.
collection PubMed
description Obesity and aging are linked to inflammation and increased risk of chronic disease. Telomeres are the endcaps of chromosomes that are regulated by telomerase, the enzyme that elongates telomeres, as well as a protein complex known as shelterin. Telomere dysfunction is associated with inflammation, aging, and disease. However, the effect of high‐fat diet (HFD) induced obesity and advancing age on the shelterin complex and telomerase in adipose tissue is unknown. The present study investigated the effects of obesity and aging on C57BL/6J mice adipose tissue mRNA expression of shelterin complex genes. Young (YG) mice (3 mo) were randomly assigned to be fed either a high‐fat diet (YG + HFD; 60% kcal from fat) or a low‐fat diet (YG + LFD; 10% kcal from fat). A subset of mice were aged until 16 months. Body weight and epididymal white adipose tissue (EWAT) weight increased with age or a HFD. There was a trend for increased Terf2 expression, as expression was increased in HFD + YG by ~47% and aged mice by ~80%. Pot1b expression was increased in aged mice by ~35%–60% compared to YG, independent of diet. mTert, the gene that codes for the catalytic subunit of telomerase, was significantly elevated in aged mice. Changes in telomere associated gene expression was accompanied by changes in expression of inflammatory markers Mcp1 and Tnfα. These findings suggest obesity and age impact expression of shelterin complex and telomerase related genes in adipose, perhaps altering telomere function in adipose tissue thereby increasing inflammation and risk of chronic disease.
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spelling pubmed-72800052020-06-10 High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue Bloom, Samuel I. Tuluca, Andrei Ives, Stephen J. Reynolds, Thomas H. Physiol Rep Original Research Obesity and aging are linked to inflammation and increased risk of chronic disease. Telomeres are the endcaps of chromosomes that are regulated by telomerase, the enzyme that elongates telomeres, as well as a protein complex known as shelterin. Telomere dysfunction is associated with inflammation, aging, and disease. However, the effect of high‐fat diet (HFD) induced obesity and advancing age on the shelterin complex and telomerase in adipose tissue is unknown. The present study investigated the effects of obesity and aging on C57BL/6J mice adipose tissue mRNA expression of shelterin complex genes. Young (YG) mice (3 mo) were randomly assigned to be fed either a high‐fat diet (YG + HFD; 60% kcal from fat) or a low‐fat diet (YG + LFD; 10% kcal from fat). A subset of mice were aged until 16 months. Body weight and epididymal white adipose tissue (EWAT) weight increased with age or a HFD. There was a trend for increased Terf2 expression, as expression was increased in HFD + YG by ~47% and aged mice by ~80%. Pot1b expression was increased in aged mice by ~35%–60% compared to YG, independent of diet. mTert, the gene that codes for the catalytic subunit of telomerase, was significantly elevated in aged mice. Changes in telomere associated gene expression was accompanied by changes in expression of inflammatory markers Mcp1 and Tnfα. These findings suggest obesity and age impact expression of shelterin complex and telomerase related genes in adipose, perhaps altering telomere function in adipose tissue thereby increasing inflammation and risk of chronic disease. John Wiley and Sons Inc. 2020-06-08 /pmc/articles/PMC7280005/ /pubmed/32512652 http://dx.doi.org/10.14814/phy2.14461 Text en © 2020 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Bloom, Samuel I.
Tuluca, Andrei
Ives, Stephen J.
Reynolds, Thomas H.
High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
title High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
title_full High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
title_fullStr High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
title_full_unstemmed High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
title_short High‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
title_sort high‐fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7280005/
https://www.ncbi.nlm.nih.gov/pubmed/32512652
http://dx.doi.org/10.14814/phy2.14461
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