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Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet

Metabolic syndrome (Mets) is an important condition because it may cause stroke and heart disease in the future. Reactive oxygen species (ROSs) influence the pathogenesis of Mets; however, the types of ROSs and their localization remain largely unknown. In this study, we investigated the effects of...

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Autores principales: Sato, Atsushi, Shiraishi, Yasunaga, Kimura, Toyokazu, Osaki, Ayumu, Kagami, Kazuki, Ido, Yasuo, Adachi, Takeshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9312060/
https://www.ncbi.nlm.nih.gov/pubmed/35883894
http://dx.doi.org/10.3390/antiox11071403
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author Sato, Atsushi
Shiraishi, Yasunaga
Kimura, Toyokazu
Osaki, Ayumu
Kagami, Kazuki
Ido, Yasuo
Adachi, Takeshi
author_facet Sato, Atsushi
Shiraishi, Yasunaga
Kimura, Toyokazu
Osaki, Ayumu
Kagami, Kazuki
Ido, Yasuo
Adachi, Takeshi
author_sort Sato, Atsushi
collection PubMed
description Metabolic syndrome (Mets) is an important condition because it may cause stroke and heart disease in the future. Reactive oxygen species (ROSs) influence the pathogenesis of Mets; however, the types of ROSs and their localization remain largely unknown. In this study, we investigated the effects of SOD1, which localize to the cytoplasm and mitochondrial intermembrane space and metabolize superoxide anion, on Mets using SOD1 deficient mice (SOD1(−/−)). SOD1(−/−) fed on a high-fat/high-sucrose diet (HFHSD) for 24 weeks showed reduced body weight gain and adipose tissue size compared to wild-type mice (WT). Insulin secretion was dramatically decreased in SOD1(−/−) fed on HFHSD even though blood glucose levels were similar to WT. Ambulatory oxygen consumption was accelerated in SOD1(−/−) with HFHSD; however, ATP levels of skeletal muscle were somewhat reduced compared to WT. Reflecting the reduced ATP, the expression of phosphorylated AMPK (Thr 172) was more robust in SOD1(−/−). SOD1 is involved in the ATP production mechanism in mitochondria and may contribute to visceral fat accumulation by causing insulin secretion and insulin resistance.
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spelling pubmed-93120602022-07-26 Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet Sato, Atsushi Shiraishi, Yasunaga Kimura, Toyokazu Osaki, Ayumu Kagami, Kazuki Ido, Yasuo Adachi, Takeshi Antioxidants (Basel) Article Metabolic syndrome (Mets) is an important condition because it may cause stroke and heart disease in the future. Reactive oxygen species (ROSs) influence the pathogenesis of Mets; however, the types of ROSs and their localization remain largely unknown. In this study, we investigated the effects of SOD1, which localize to the cytoplasm and mitochondrial intermembrane space and metabolize superoxide anion, on Mets using SOD1 deficient mice (SOD1(−/−)). SOD1(−/−) fed on a high-fat/high-sucrose diet (HFHSD) for 24 weeks showed reduced body weight gain and adipose tissue size compared to wild-type mice (WT). Insulin secretion was dramatically decreased in SOD1(−/−) fed on HFHSD even though blood glucose levels were similar to WT. Ambulatory oxygen consumption was accelerated in SOD1(−/−) with HFHSD; however, ATP levels of skeletal muscle were somewhat reduced compared to WT. Reflecting the reduced ATP, the expression of phosphorylated AMPK (Thr 172) was more robust in SOD1(−/−). SOD1 is involved in the ATP production mechanism in mitochondria and may contribute to visceral fat accumulation by causing insulin secretion and insulin resistance. MDPI 2022-07-19 /pmc/articles/PMC9312060/ /pubmed/35883894 http://dx.doi.org/10.3390/antiox11071403 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Sato, Atsushi
Shiraishi, Yasunaga
Kimura, Toyokazu
Osaki, Ayumu
Kagami, Kazuki
Ido, Yasuo
Adachi, Takeshi
Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet
title Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet
title_full Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet
title_fullStr Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet
title_full_unstemmed Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet
title_short Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet
title_sort resistance to obesity in sod1 deficient mice with a high-fat/high-sucrose diet
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9312060/
https://www.ncbi.nlm.nih.gov/pubmed/35883894
http://dx.doi.org/10.3390/antiox11071403
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