title: Moderate exercise improves leucocyte function and decreases inflammation in diabetes.
abstract: The genesis and progression of diabetes occur due in part to an uncontrolled inflammation profile with insulin resistance, increased serum levels of free fatty acids (FFA), proinflammatory cytokines and leucocyte dysfunction. In this study, an investigation was made of the effect of a 3-week moderate exercise regimen on a treadmill (60% of VO₂(max) , 30 min/day, 6 days a week) on inflammatory markers and leucocyte functions in diabetic rats. The exercise decreased serum levels of tumour necrosis factor (TNF)-α (6%), cytokine-induced neutrophil chemotactic factor 2 alpha/beta (CINC-2α/β) (9%), interleukin (IL)-1β (34%), IL-6 (86%), C-reactive protein (CRP) (41%) and FFA (40%) in diabetic rats when compared with sedentary diabetic animals. Exercise also attenuated the increased responsiveness of leucocytes from diabetics when compared to controls, diminishing the reactive oxygen species (ROS) release by neutrophils (21%) and macrophages (28%). Exercise did not change neutrophil migration and the proportion of neutrophils and macrophages in necrosis (loss of plasma membrane integrity) and apoptosis (DNA fragmentation). Serum activities of creatine kinase (CK) and lactate dehydrogenase (LDH) were not modified in the conditions studied. Therefore, physical training did not alter the integrity of muscle cells. We conclude that moderate physical exercise has marked anti-inflammatory effects on diabetic rats. This may be an efficient strategy to protect diabetics against microorganism infection, insulin resistance and vascular complications.
authors.affiliation: Cruzeiro do Sul University, Brazil.
authors.forename: M F
authors.initials: MF
authors.lastname: Belotto
authors.forename: J
authors.initials: J
authors.lastname: Magdalon
authors.forename: H G
authors.initials: HG
authors.lastname: Rodrigues
authors.forename: M A R
authors.initials: MA
authors.lastname: Vinolo
authors.forename: R
authors.initials: R
authors.lastname: Curi
authors.forename: T C
authors.initials: TC
authors.lastname: Pithon-Curi
authors.forename: E
authors.initials: E
authors.lastname: Hatanaka
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D002097:C-Reactive Protein / Q000378:metabolism; D019743:Chemokines, CXC / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D016207:Cytokines / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000276:immunology* / Q000628:therapy; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000276:immunology / Q000628:therapy; D005230:Fatty Acids, Nonesterified / Q000097:blood; D007249:Inflammation / Q000097:blood / Q000276:immunology; D007378:Interleukins / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007962:Leukocytes / Q000276:immunology* / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D009336:Necrosis / Q000276:immunology / Q000473:pathology; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010529:Peritoneal Cavity / Q000166:cytology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D019743:Chemokines, CXC; C513294:Cxcl3 protein, rat; D016207:Cytokines; D005230:Fatty Acids, Nonesterified; D007378:Interleukins; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D013755:Tetradecanoylphorbol Acetate