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This Article Full Text Full Text (PDF) Supplementary figures 1 & 2 All Versions of this Article: JOE-08-0387v1 200/2/151    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chen, H.-S. Articles by Lin, H.-D. Search for Related Content PubMed PubMed Citation Articles by Chen, H.-S. Articles by Lin, H.-D.

¹ Division of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital, No. 201, Shih-Pai Road, Sec 2, Taipei 11217, Taiwan, ROC² Department of Medicine, National Yang-Ming University School of Medicine, Taipei 11227, Taiwan, ROC³ Institute of Physiology, National Yang-Ming University School of Medicine, Taipei 11227, Taiwan, ROC

(Correspondence should be addressed to H-S Chen; Email: chenhs{at}vghtpe.gov.tw)

Heat shock protein 60 (HSPD1) plays a critical role in myocardial protection. Its reduced expression may lower myocardial protection against ischemic injury in the diabetic state. This study was conducted to investigate the natural course of fructose-fed insulin-resistant rats, define changes in myocardial HSPD1 expression, and determine the effects of thiazolidinedione or anti-hypertensive treatment. Results showed that insulin resistance with hyperinsulinemia and hypertension developed after 6 weeks of fructose feeding. This time-course study also showed that myocardial HSPD1 expression was mildly increased in week 6 (P=0.05) and significantly increased in week 8. Rosiglitazone-treated rats had restored systolic blood pressure (BP) and normalized plasma insulin level during oral glucose tolerance tests, whereas amlodipine-treated rats restored only systolic BP. Both amlodipine and rosiglitazone treatments normalized the abundance of myocardial HSPD1 expression in fructose-fed rats. When these rats received streptozotocin injection and diabetes developed, myocardial HSPD1 expression decreased despite persistent hypertension. In conclusion, this is the first study to report that myocardial HSPD1 expression is increased in high-fructose-fed rats, which may be due to increased BP. Once the high-fructose-fed rats developed diabetes with insulin deficiency, the myocardial HSPD1 expression decreased in spite of persistent hypertension.