Premium
Antioxidant treatment with tempol prevents obesity induced remodeling of middle cerebral arteries in Sprague‐Dawley rats
Author(s) -
Pires Paulo W,
McClain Jonathon L,
Dorrance Anne M
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.613.12
Subject(s) - myograph , medicine , endocrinology , oxidative stress , middle cerebral artery , antioxidant , cerebral arteries , lumen (anatomy) , diabetes mellitus , obesity , chemistry , artery , biochemistry , ischemia
Obesity is a risk factor for stroke, especially when associated with diabetes. Cerebral vessel remodeling may contribute to this increased risk of cerebrovascular accidents. We hypothesized that a diet rich in fat and carbohydrates would contribute to middle cerebral artery (MCA) remodeling, and that oxidative stress would play a key role in the process. Three week old male Sprague‐Dawley rats were fed a high‐fat (HF) diet containing 36% fat and 36% carbohydrate (n=21), or HF plus the super oxide dismutase mimetic, tempol (n=9) or regular chow (n= 18) for 18 weeks. MCA's were mounted in a pressure myograph under calcium‐free conditions to assess vascular structure. All data are shown as mean±SEM. Body weight was higher in the groups that received HF diet (442±6, 484±19, 374±9 grams, HF, HF+tempol and control); the same was true for visceral fat weight (16.2±0.9, 22.1±3.1, 5.7±0.5 grams, HF, HF+tempol, control). Blood glucose was increased in the HF group (197±10, 143±5 mg/dl, HF vs control) and treatment with tempol reversed this effect (115±10 mg/dl). Wall/lumen ratio was higher in the HF rats and reduced by tempol treatment (0.15±0.02, 0.08±0.01, 0.08±0.01, HF, HF+tempol, control, at 80mmHg p<0.05), the same was true for wall thickness and wall area. These results suggest that a HF diet increases MCA remodeling and blood glucose, and tempol treatment reverses these processes. ADA‐7‐07‐RA28, AHA‐0840122N