Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hong, So-hyeon | - |
dc.contributor.author | Choi, Kyung Mook | - |
dc.date.accessioned | 2021-08-31T14:43:19Z | - |
dc.date.available | 2021-08-31T14:43:19Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2020-01-02 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/58357 | - |
dc.description.abstract | The prevalence of sarcopenic obesity is increasing worldwide, particularly amongst aging populations. Insulin resistance is the core mechanism of sarcopenic obesity and is also associated with variable cardiometabolic diseases such as cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. Fat accumulation in muscle tissue promotes a proinflammatory cascade and oxidative stress, leading to mitochondrial dysfunction, impaired insulin signaling, and muscle atrophy. To compound the problem, decreased muscle mass aggravates insulin resistance. In addition, the crosstalk between myokines and adipokines leads to negative feedback, which in turn aggravates sarcopenic obesity and insulin resistance. In this review, we focus on the molecular mechanisms linking sarcopenic obesity and insulin resistance with various biological pathways. We also discuss the impact and mechanism of sarcopenic obesity and insulin resistance on cardiometabolic disease. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.subject | HUMAN SKELETAL-MUSCLE | - |
dc.subject | FATTY LIVER-DISEASE | - |
dc.subject | PROTEIN-KINASE-C | - |
dc.subject | ADIPOSE-TISSUE | - |
dc.subject | HEART-FAILURE | - |
dc.subject | SIGNALING PATHWAYS | - |
dc.subject | DYNAPENIC OBESITY | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | BODY-COMPOSITION | - |
dc.subject | ACID-METABOLISM | - |
dc.title | Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, Kyung Mook | - |
dc.identifier.doi | 10.3390/ijms21020494 | - |
dc.identifier.scopusid | 2-s2.0-85077942123 | - |
dc.identifier.wosid | 000515380000124 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.21, no.2 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 21 | - |
dc.citation.number | 2 | - |
dc.type.rims | ART | - |
dc.type.docType | Review | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.subject.keywordPlus | HUMAN SKELETAL-MUSCLE | - |
dc.subject.keywordPlus | FATTY LIVER-DISEASE | - |
dc.subject.keywordPlus | PROTEIN-KINASE-C | - |
dc.subject.keywordPlus | ADIPOSE-TISSUE | - |
dc.subject.keywordPlus | HEART-FAILURE | - |
dc.subject.keywordPlus | SIGNALING PATHWAYS | - |
dc.subject.keywordPlus | DYNAPENIC OBESITY | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | BODY-COMPOSITION | - |
dc.subject.keywordPlus | ACID-METABOLISM | - |
dc.subject.keywordAuthor | sarcopenic obesity | - |
dc.subject.keywordAuthor | insulin resistance | - |
dc.subject.keywordAuthor | cardiometabolic disease | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.