Metabolic syndrome (high cholesterol, triglycerides, high blood sugar & high blood pressure) is induced by physical inactivity and consumption of a diet high in fat and refined sugar, which generates obesity and excess belly fat. Recent evidence suggest that oxidative stress is elevated in those with metabolic syndrome. Hypertension is associated with oxidative stress, due to nitric oxide inactivation, and down-regulation of nitric oxide synthase isoforms and endothelial nitric oxide activator.
In non-diabetic individuals, lipid peroxidation (oxidized rancid fats), represented by plasma thiobarbituric acid and urinary 8-epi-prostaglandin-F2α , are positively correlated with body mass index and waist circumference. This indicates that fat accumulation is correlated with oxidative stress.
Data from 2,002 non-diabetic subjects of the Framingham Offspring Study showed that systemic oxidative stress is associated with insulin resistance. Insulin resistance induces an impairment in phosphatidylinositol 3-kinase (PI3K) dependent signaling, which in the blood vessels protective lining (the endothelium) may cause imbalance between production of nitric oxide (blood vessel widening molecule) and secretion of endothelin-1 (blood vessel tightening peptide), leading to endothelial dysfunction.
Epidemiological studies strongly support a reciprocal relationship between endothelial dysfunction, which contributes to development of hypertension, and insulin resistance. In a prospective cohort study, each one-unit decrease of flow-mediated dilatation was associated with a significant 16% increase in the relative risk of incident hypertension, suggesting that an impaired endothelial vasomotor function precedes and predicts the future development of hypertension.
Adipose (fat) tissue is a major endocrine organ that secrets a variety of bioactive substances.
Obesity and excess belly fat generate oxidative stress which leads to impaired endothelial function and thus the development of hypertension. Less body fat helps reduce the oxidative stress bioactive mechanisms that contribute to hypertension.
Sources:
Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study.
Meigs JB, Larson MG
Diabetes Care 2007, 30:2529-2535
Reciprocal relationships between insulin resistance and endothelial dysfunction: molecular and pathophysiological mechanisms.
Kim JA, Montagnani M, Koh KK, Quon MJ
Circulation 2006, 113:1888-1904
The underlying mechanisms for the development of hypertension in the metabolic syndrome
Hidekatsu Yana, Yoshiharu Tomona
Nutrition Journal 2008
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