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Exercise Training Improves Endothelial Dysfunction in Type 2 Diabetes
Author(s) -
Lee Sewon,
Park Yoonjung,
Zhang Cuihua
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.594.4
Subject(s) - medicine , vasodilation , endothelial dysfunction , type 2 diabetes , endocrinology , endothelium , sodium nitroprusside , aerobic exercise , insulin resistance , diabetes mellitus , nitric oxide , cardiology
Type 2 diabetes (T2D) is a leading risk factor for cardiovascular diseases including peripheral artery disease and coronary heart disease. Exercise training (ET) is thought to have a beneficial effect on these disorders, but the basis for this effect is not fully understood. Because endothelial function (EF) and insulin resistance (IR) play key roles in the pathological events leading to vascular disease in T2D, we hypothesized that the ET will exert its effects on improving EF and IR. To test this hypothesis, we assessed the effects of ET in vascular function of diabetic (db/db, BKS.Cg‐m+/+Leprdb/J) mice by evaluating EF of isolated coronary arterioles of wild‐type (WT, C57B/J) and db/db with/without ET. Although dilation of vessels to the endothelium‐independent vasodilator, sodium nitroprusside was not different between db/db and WT, dilation to the endothelium‐dependent agonist, acetylcholine (ACh) was impaired in db/db (n=12, P<0.01) compare to WT (n=8). However, vasodilation to ACh was restored in db/db with ET (n=8). In addition, IR was improved in the db/db after ET. ET did not change body weight of db/db, but superoxide dismutase (SOD1 and SOD2) protein expression of heart tissue was up‐regulated by over 40% by ET. Although we have not yet linked the exercise‐induced increase in anti‐oxidants to the improvement in EF in T2D, we suggest that this connection may be the basis for the benefit of ET in T2D.