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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Veröffentlicht in:Experimental diabetes research 2012-01, Vol.2012 (2012), p.1-7
Hauptverfasser: Kadowaki, Shinpei, Kiribayashi, Nobuyuki, Shishido, Tetsuro, Narumi, Taro, Nishiyama, Satoshi, Takahashi, Hiroki, Arimoto, Takanori, Miyashita, Takehiko, Miyamoto, Takuya, Watanabe, Tetsu, Shibata, Yoko, Konta, Tsuneo, Ueno, Yoshiyuki, Kato, Takeo, Kayama, Takamasa, Kubota, Isao
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Sprache:eng
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Zusammenfassung: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.
ISSN:1687-5214
1687-5303
DOI:10.1155/2012/815098