title: Training alters the skeletal muscle antioxidative capacity in non-insulin-dependent type 2 diabetic men.
abstract: The present study analyzes the oxidative stress situation in the skeletal muscle of overweight/obese men suffering from non-insulin-dependent type 2 diabetes mellitus [T2DM, n=16, years=61±7, body mass index (BMI)=31±4 kg/m(2) ] and BMI-matched non-diabetic male control subjects (CON, n=7, years=53±6, BMI=30±4 kg/m(2) ). Furthermore, it investigates whether physical training can alter the skeletal muscle antioxidative capacity of T2DM patients at rest. Molecule content analyses (immunohistochemical stainings) of 8-iso-prostaglandin-F2α (8-Iso-PGF), superoxide dismutase-2 (SOD2), glutathione peroxidase-1 (GPX1), peroxiredoxin isoforms (PRDX 1-6) and heat-shock-protein-70 (HSP70) were performed in biopsies taken from the vastus lateralis muscle. Under basal conditions, 8-Iso-PGF was significantly decreased in T2DM patients (-35.7%), whereas PRDX2 and PRDX6 were significantly increased relative to CON (+82.6%; +82.3%). Differences were neither observed in SOD2 nor in GPX1 or PRDX1, 3, 4, 5 density. Regular physical activity (moderate endurance or resistance training twice a week for 3 months) did not alter PRDX1, 2, 3, 4, 6 in the skeletal muscle of T2DM patients, but significantly increased SOD2 (+65.9%), GPX1 (+62.4%), PRDX5 (+37.5%), and HSP70 (+48.5%). Overweight/obese men with non-insulin-dependent T2DM exhibit up-regulated cytosolic peroxiredoxin contents relative to BMI-matched controls. Regular training further up-regulates cytosolic and mitochondrial antioxidative enzymes in T2DM patients and improves their cellular protection systems. This may contribute to a retardation of the disease's progression.
authors.affiliation: Department of Molecular and Cellular Sport Medicine, Institute of Cardiovascular Research and Sport Medicine, German Sport University Cologne, Cologne, Germany. ch.brinkmann@gmx.net
authors.forename: C
authors.initials: C
authors.lastname: Brinkmann
authors.forename: N
authors.initials: N
authors.lastname: Chung
authors.forename: U
authors.initials: U
authors.lastname: Schmidt
authors.forename: T
authors.initials: T
authors.lastname: Kreutz
authors.forename: E
authors.initials: E
authors.lastname: Lenzen
authors.forename: T
authors.initials: T
authors.lastname: Schiffer
authors.forename: S
authors.initials: S
authors.lastname: Geisler
authors.forename: C
authors.initials: C
authors.lastname: Graf
authors.forename: G
authors.initials: G
authors.lastname: Montiel-Garcia
authors.forename: R
authors.initials: R
authors.lastname: Renner
authors.forename: W
authors.initials: W
authors.lastname: Bloch
authors.forename: K
authors.initials: K
authors.lastname: Brixius
mesh_terms: D000368:Aged; D015992:Body Mass Index; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism / Q000534:rehabilitation*; D005081:Exercise Therapy; D005979:Glutathione Peroxidase / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000534:rehabilitation*; D050177:Overweight / Q000150:complications / Q000378:metabolism / Q000534:rehabilitation; D054464:Peroxiredoxins / Q000378:metabolism; D017382:Reactive Oxygen Species; D055070:Resistance Training; D013482:Superoxide Dismutase / Q000378:metabolism; D000094765:Glutathione Peroxidase GPX1; D000099156:Superoxide Dismutase 2
chemical_list: D005979:Glutathione Peroxidase; D018840:HSP70 Heat-Shock Proteins; D054464:Peroxiredoxins; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D000094765:Glutathione Peroxidase GPX1; D000099156:Superoxide Dismutase 2; C000722067:GPX1 protein, human