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Acute exercise induces oxidative stress, whereas exercise training up\u2010regulates endogenous antioxidant defenses and <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content> expression. Although diabetic nephropathy is a major contributor to diabetic morbidity, information regarding the effect of <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>s on kidney protection is limited. This study evaluated the effects of eight\u2010week exercise training on kidney <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content> expression and markers of oxidative stress at rest and after acute exercise in rats with or without streptozotocin\u2010induced diabetes. Induction of diabetes increased <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\u2010binding activity of heat shock factor\u20101, but decreased the expression of <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>72, <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>60, and <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>90. The inflammatory markers <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 and <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010alpha were increased in the kidney tissue of diabetic animals. Both exercise training and acute exercise increased <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>72 and <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>90 protein levels only in non\u2010diabetic rats. On the other hand, exercise training appeared to reverse the diabetes\u2010induced histological changes together with decreased expression of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010beta as a key inducer of glomerulosclerosis, and decreased levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 and <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010alpha. Notably, <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>72 and <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010beta were negatively correlated. In conclusion, impaired <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content> defense seems to contribute to kidney injury vulnerability in diabetes and exercise training does not up\u2010regulate kidney <jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content> expression despite the improvements in histopathological and inflammatory markers.<\/jats:p>","DOI":"10.1111\/sms.13079","type":"journal-article","created":{"date-parts":[[2018,2,23]],"date-time":"2018-02-23T20:11:45Z","timestamp":1519416705000},"page":"1808-1817","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Suppressed heat shock protein response in the kidney of exercise\u2010trained diabetic rats"],"prefix":"10.1111","volume":"28","author":[{"given":"J.","family":"Lappalainen","sequence":"first","affiliation":[{"name":"Institute of Biomedicine, Physiology University of Eastern Finland  Kuopio Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N. 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