title: Decreased thioredoxin-1 and increased HSP90 expression in skeletal muscle in subjects with type 2 diabetes or impaired glucose tolerance.
abstract: In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n = 10) were compared with subjects with impaired glucose tolerance (IGT) (n = 8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P = 0.031) and HSP90 was 380% higher (P < 0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research.
authors.affiliation: Institute of Biomedicine, Exercise Medicine, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
authors.forename: M
authors.initials: M
authors.lastname: Venojärvi
authors.affiliation: Institute of Biomedicine, Physiology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
authors.forename: A
authors.initials: A
authors.lastname: Korkmaz
authors.affiliation: Department of Health, Functional Capacity and Welfare, Functional Capacity Unit, National Institute for Health and Welfare, 20720 Turku, Finland.
authors.forename: S
authors.initials: S
authors.lastname: Aunola
authors.affiliation: PET Centre, University of Turku, 20520 Turku, Finland.
authors.forename: K
authors.initials: K
authors.lastname: Hällsten
authors.affiliation: PET Centre, University of Turku, 20520 Turku, Finland.
authors.forename: K
authors.initials: K
authors.lastname: Virtanen
authors.affiliation: Department of Chronic Disease Prevention, Population Studies Unit, National Institute for Health and Welfare, 20520 Turku, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Marniemi
authors.affiliation: Social Insurance Institution, Research Department, 20720 Turku, Finland.
authors.forename: J-P
authors.initials: JP
authors.lastname: Halonen
authors.affiliation: Institute of Biomedicine, Physiology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
authors.forename: O
authors.initials: O
authors.lastname: Hänninen
authors.affiliation: PET Centre, University of Turku, 20520 Turku, Finland.
authors.forename: P
authors.initials: P
authors.lastname: Nuutila
authors.affiliation: Institute of Biomedicine, Physiology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
authors.forename: M
authors.initials: M
authors.lastname: Atalay
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000473:pathology; D005260:Female; D018149:Glucose Intolerance / Q000378:metabolism* / Q000473:pathology; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D018841:HSP90 Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D013879:Thioredoxins / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D050884:HSP72 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; D013879:Thioredoxins