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Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study

Background. Insulin resistance (IR) is part of the metabolic syndrome (Mets) that develops after lifestyle changes and obesity. Although the association between Mets and myocardial injury is well known, the effect of IR on myocardial damage remains unclear. Methods and Results. We studied 2200 norma...

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Autores principales: Narumi, Taro, Shishido, Tetsuro, Kiribayashi, Nobuyuki, Kadowaki, Shinpei, Nishiyama, Satoshi, Takahashi, Hiroki, Arimoto, Takanori, Miyashita, Takehiko, Miyamoto, Takuya, Watanabe, Tetsu, Shibata, Yoko, Konta, Tsuneo, Ueno, Yoshiyuki, Kato, Takeo, Kayama, Takamasa, Kubota, Isao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3474255/
https://www.ncbi.nlm.nih.gov/pubmed/23093954
http://dx.doi.org/10.1155/2012/815098
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author Narumi, Taro
Shishido, Tetsuro
Kiribayashi, Nobuyuki
Kadowaki, Shinpei
Nishiyama, Satoshi
Takahashi, Hiroki
Arimoto, Takanori
Miyashita, Takehiko
Miyamoto, Takuya
Watanabe, Tetsu
Shibata, Yoko
Konta, Tsuneo
Ueno, Yoshiyuki
Kato, Takeo
Kayama, Takamasa
Kubota, Isao
author_facet Narumi, Taro
Shishido, Tetsuro
Kiribayashi, Nobuyuki
Kadowaki, Shinpei
Nishiyama, Satoshi
Takahashi, Hiroki
Arimoto, Takanori
Miyashita, Takehiko
Miyamoto, Takuya
Watanabe, Tetsu
Shibata, Yoko
Konta, Tsuneo
Ueno, Yoshiyuki
Kato, Takeo
Kayama, Takamasa
Kubota, Isao
author_sort Narumi, Taro
collection PubMed
description Background. Insulin resistance (IR) is part of the metabolic syndrome (Mets) that develops after lifestyle changes and obesity. Although the association between Mets and myocardial injury is well known, the effect of IR on myocardial damage remains unclear. Methods and Results. We studied 2200 normal subjects who participated in a community-based health check in the town of Takahata in northern Japan. The presence of IR was assessed by homeostasis model assessment ratio, and the serum level of heart-type fatty acid binding protein (H-FABP) was measured as a maker of silent and ongoing myocardial damage. H-FABP levels were significantly higher in subjects with IR and Mets than in those without metabolic disorder regardless of gender. Multivariate logistic analysis showed that the presence of IR was independently associated with latent myocardial damage (odds ratio: 1.574, 95% confidence interval 1.1–2.3) similar to the presence of Mets. Conclusions. In a screening of healthy subjects, IR and Mets were similarly related to higher H-FABP levels, suggesting that there may be an asymptomatic population in the early stages of metabolic disorder that is exposed to myocardial damage and might be susceptible to silent heart failure.
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spelling pubmed-34742552012-10-23 Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study Narumi, Taro Shishido, Tetsuro Kiribayashi, Nobuyuki Kadowaki, Shinpei Nishiyama, Satoshi Takahashi, Hiroki Arimoto, Takanori Miyashita, Takehiko Miyamoto, Takuya Watanabe, Tetsu Shibata, Yoko Konta, Tsuneo Ueno, Yoshiyuki Kato, Takeo Kayama, Takamasa Kubota, Isao Exp Diabetes Res Clinical Study Background. Insulin resistance (IR) is part of the metabolic syndrome (Mets) that develops after lifestyle changes and obesity. Although the association between Mets and myocardial injury is well known, the effect of IR on myocardial damage remains unclear. Methods and Results. We studied 2200 normal subjects who participated in a community-based health check in the town of Takahata in northern Japan. The presence of IR was assessed by homeostasis model assessment ratio, and the serum level of heart-type fatty acid binding protein (H-FABP) was measured as a maker of silent and ongoing myocardial damage. H-FABP levels were significantly higher in subjects with IR and Mets than in those without metabolic disorder regardless of gender. Multivariate logistic analysis showed that the presence of IR was independently associated with latent myocardial damage (odds ratio: 1.574, 95% confidence interval 1.1–2.3) similar to the presence of Mets. Conclusions. In a screening of healthy subjects, IR and Mets were similarly related to higher H-FABP levels, suggesting that there may be an asymptomatic population in the early stages of metabolic disorder that is exposed to myocardial damage and might be susceptible to silent heart failure. Hindawi Publishing Corporation 2012 2012-10-10 /pmc/articles/PMC3474255/ /pubmed/23093954 http://dx.doi.org/10.1155/2012/815098 Text en Copyright © 2012 Taro Narumi et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Clinical Study
Narumi, Taro
Shishido, Tetsuro
Kiribayashi, Nobuyuki
Kadowaki, Shinpei
Nishiyama, Satoshi
Takahashi, Hiroki
Arimoto, Takanori
Miyashita, Takehiko
Miyamoto, Takuya
Watanabe, Tetsu
Shibata, Yoko
Konta, Tsuneo
Ueno, Yoshiyuki
Kato, Takeo
Kayama, Takamasa
Kubota, Isao
Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study
title Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study
title_full Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study
title_fullStr Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study
title_full_unstemmed Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study
title_short Impact of Insulin Resistance on Silent and Ongoing Myocardial Damage in Normal Subjects: The Takahata Study
title_sort impact of insulin resistance on silent and ongoing myocardial damage in normal subjects: the takahata study
topic Clinical Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3474255/
https://www.ncbi.nlm.nih.gov/pubmed/23093954
http://dx.doi.org/10.1155/2012/815098
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