title: Exercise training improves acetylcholine-induced endothelium-dependent hyperpolarization in type 2 diabetic rats, Otsuka Long-Evans Tokushima fatty rats.
abstract: We investigated whether endothelium-derived relaxing (EDRF) and hyperpolarizing factor (EDHF) is impaired in type 2 diabetic rats (Otsuka Long-Evans Tokushima Fatty (OLETF) rat) and whether the exercise training improves impaired EDRF and EDHF. Diabetic rats were divided into the sedentary and exercise-trained groups at the age of 16 weeks. Long-Evans Tokushima Otsuka (LETO) rats were used as age-matched non-diabetic controls. EDRF as well as EDHF induced by acetylcholine in the presence of indomethacine and L-nitro N-arginine was significantly attenuated in the diabetic rats, and was further impaired with age. Exercise training significantly improved it. Both insulin resistance and abdominal fat accumulation were significantly greater in the diabetic rats, compared with the non-diabetic rats, but were decreased in exercise-trained rats. Urinary NO(2) secretion was decrease in the diabetic rats at each age, and it was improved by exercise training. The results of the study indicated that exercise training prevented impairment of EDHF, as well as EDRF in type 2 diabetic rats, presumably due to improvement of hyperglycemia and insulin resistance and increase in the production of nitric oxide by exercise training.
authors.affiliation: Department of Nutrition, School of Medicine, University of Tokushima, 3-18-15, Kuramoto-cho, Tokushima 770-8503, Japan.
authors.forename: Asako
authors.initials: A
authors.lastname: Minami
authors.forename: Noriko
authors.initials: N
authors.lastname: Ishimura
authors.forename: Nagakatsu
authors.initials: N
authors.lastname: Harada
authors.forename: Sadaichi
authors.initials: S
authors.lastname: Sakamoto
authors.forename: Yasuharu
authors.initials: Y
authors.lastname: Niwa
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Nakaya
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000367:Age Factors; D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism; D001013:Aorta, Thoracic / Q000378:metabolism; D001685:Biological Factors / Q000502:physiology*; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology / Q000628:therapy*; D004195:Disease Models, Animal; D004435:Eating / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D005081:Exercise Therapy; D006632:Histamine / Q000494:pharmacology; D008055:Lipids / Q000097:blood; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects; D009569:Nitric Oxide / Q000502:physiology* / Q000652:urine; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D020334:Rats, Inbred OLETF; D016212:Transforming Growth Factor beta / Q000096:biosynthesis; D053773:Transforming Growth Factor beta1; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D001685:Biological Factors; D001786:Blood Glucose; D008055:Lipids; D012333:RNA, Messenger; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D006632:Histamine; D000109:Acetylcholine