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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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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. |
format | Online Article Text |
id | pubmed-9312060 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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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