Key result
A methionine-enriched diet for 48 weeks induced metabolic disturbances, increased collagen deposition in coronary and carotid arteries, and decreased PPARγ expression in coronary arterioles in rats.
May link hyperhomocysteinemia to vascular remodeling via oxidative stress and reduced PPARγ; leaves open any clinical role pending human data.
Hyperhomocysteinemia, a risk factor for vascular disease, is associated with metabolic syndrome. Our study was aimed at exploring the effect of long-term hyperhomocysteinemia with metabolic disturbances on vascular remodeling. We also studied oxidative stress and expression of PPARγin the coronary arteriole as a possible mechanism underlying vascular remodeling. Rats were treated with standard rodent chow (Control) or diet enriched in methionine (Met) for 48 weeks. Plasma homocysteine, blood glucose, serum lipids, malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels were measured. Coronary arteriolar and carotid arterial remodeling was assessed by histomorphometric techniques and the expression of PPARγin vessel wall was investigated. In Met group, an increase in the level of fasting blood glucose, serum triglyceride, total cholesterol, MDA, and NO, a decline in the serum SOD level, and increased collagen deposition in coronary and carotid arteries were found. Moreover, we detected decreased expression of PPARγin the coronary arterioles in Met group. In summary, our study revealed metabolic disturbances in this model of long-term hyperhomocysteinemia together with vascular remodeling and suggested that impaired oxidative stress, endothelium dysfunction, and decreased PPARγexpression in the vessel wall could be underlying mechanisms.
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Huo et al. (2018) studied Hyperhomocysteinemia with metabolic disturbance. Diet enriched in methionine vs. Standard rodent chow was evaluated on Vascular remodeling, oxidative stress, and PPARγ expression. A methionine-enriched diet for 48 weeks induced metabolic disturbances, increased collagen deposition in coronary and carotid arteries, and decreased PPARγ expression in coronary arterioles in rats.
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