Key result
In high-fat-diet-induced obese dogs, acetylcholine-induced nitric oxide production was significantly impaired after 8 months compared to baseline (1.0 vs 2.6 nmol/L, P=0.03), while coronary flow response was preserved.
Why the study?
Does a high-fat diet impair coronary endothelial function and nitric oxide production in adult mongrel dogs?
Does a high-fat diet impair coronary endothelial function and nitric oxide production in adult mongrel dogs?
Direct in vivo measurement using a catheter-type NO sensor demonstrates that a high-fat diet impairs coronary nitric oxide production in dogs before coronary flow responses to acetylcholine are affected.
BACKGROUND: Direct measurement of plasma nitric oxide (NO) concentration is possible with a newly developed catheter-type sensor. METHODS AND RESULTS: Adult mongrel dogs (n=5) were fed a high-fat diet (120 kcal . kg(-1) . day(-1)) for 8 months, then endothelial function was assessed by the change in NO concentration induced by acetylcholine (ACh) (DeltaNO). Simultaneously, average peak velocity (APV) was obtained by Doppler guide wire. Although fasting plasma glucose levels did not change after high-fat diet, fasting plasma insulin levels increased significantly (103+/-36 vs 106+/-27 mg/dl, P=0.89 and 0.15+/-0.15 vs 0.26+/-0.07 ng/ml, P=0.04, respectively). ACh-induced peak APV after high-fat feeding was not significantly different from that at baseline (ACh 0.1 microg/kg; 43+/-17 vs 51+/-7 cm/s, P=NS, ACh 0.4 microg/kg; 45+/-20 vs 47+/-16 cm/s, P=NS, respectively). The DeltaNO was significantly smaller after high-fat diet than at baseline (ACh 0.1 microg/kg; 2.6+/-1.6 vs 1.0+/-0.5 nmol/L, P=0.03, ACh 0.4 microg/kg; 3.8+/-2.3 vs 1.8+/-1.1 nmol/L, P=0.04, respectively). CONCLUSIONS: In high-fat-diet-induced obese dogs NO production was impaired in the early stage when the coronary flow response to ACh may be preserved.
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Kume et al. (2009) studied Obesity and coronary endothelial dysfunction (n=8). High-fat diet vs. Baseline / Regular diet was evaluated on Change in NO concentration induced by acetylcholine (0.1 μg/kg) (p=0.03). In high-fat-diet-induced obese dogs, acetylcholine-induced nitric oxide production was significantly impaired after 8 months compared to baseline (1.0 vs 2.6 nmol/L, P=0.03), while coronary flow response was preserved.
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