Abstract
BackgroundInsulin resistance, which is associated with an increased risk of cardiovascular morbidity and mortality, has become a leading nutrition problem. Inorganic nitrate enriched in spinach has been demonstrated to reverse the pathological features of insulin resistance and endothelial dysfunction. However, the effects of a direct intake of nitrate-enriched spinach on insulin resistance and endothelial dysfunction have not been studied.ObjectiveTo investigate the effects of spinach nitrate on insulin resistance, lipid metabolism, endothelial function, and inflammation in mice fed with a high-fat and high-fructose diet.DesignA diet intervention of spinach with or without nitrate was performed in mice. A high-fat and high-fructose diet was used to cause insulin resistance, endothelial dysfunction, and inflammation in mice. The impacts of spinach nitrate on lipid profile, insulin resistance, markers of endothelial function, and inflammation were determined in mice.ResultsSpinach nitrate improved the vascular endothelial function of the mice with high-fat and high-fructose consumption, as evidenced by the elevated plasma nitrite level, increased serum nitric oxide (NO) level and decreased serum ET-1 level after spinach nitrate intervention. Spinach nitrate also reduced serum triglycerides, total cholesterol, and low-density lipoprotein-cholesterol levels and elevated serum high-density lipoprotein-cholesterol levels in the mice fed with a high-fat and high-fructose diet. Mice receiving spinach with 60 mg/kg of nitrate (1.02±0.34) showed a significantly low homeostasis model assessment-insulin resistance index as compared with the model mice (2.05±0.58), which is indicating that spinach nitrate could effectively improve the insulin resistance. In addition, spinach nitrate remarkably decreased the elevated serum C-reactive protein, tumor necrosis factor α, and interleukin-6 levels induced by a high-fat and high-fructose diet.ConclusionsThe intake of spinach nitrate can augment NO status, improve lipid homeostasis, relieve inflammation, and enhance endothelial function, suggesting that spinach is promising dietary supplements for insulin resistance prevention.
Highlights
Insulin resistance, which is associated with an increased risk of cardiovascular morbidity and mortality, has become a leading nutrition problem
Effect of spinach nitrate ingestion on plasma nitrite, serum endothelin 1 (ET-1), nitric oxide (NO) levels, and nitric oxide synthase (NOS) activity Figure 1 shows the plasma nitrite levels in mice receiving the processed spinach with different doses of nitrate measured by gas-phase chemiluminescence assay
The serum ET-1 level in mice decreased after giving nitrate-rich spinach for 28 days, where it dropped from 5.1890.88 ng/L for the model group to 4.3490.86 ng/L(p!0.05), 4.0190.57 ng/L, and 3.5090.69 ng/L for the low, medium, and high-dose groups, respectively
Summary
Insulin resistance, which is associated with an increased risk of cardiovascular morbidity and mortality, has become a leading nutrition problem. The effects of a direct intake of nitrate-enriched spinach on insulin resistance and endothelial dysfunction have not been studied. Objective: To investigate the effects of spinach nitrate on insulin resistance, lipid metabolism, endothelial function, and inflammation in mice fed with a high-fat and high-fructose diet. The impacts of spinach nitrate on lipid profile, insulin resistance, markers of endothelial function, and inflammation were determined in mice. Results: Spinach nitrate improved the vascular endothelial function of the mice with high-fat and highfructose consumption, as evidenced by the elevated plasma nitrite level, increased serum nitric oxide (NO) level and decreased serum ET-1 level after spinach nitrate intervention. Conclusions: The intake of spinach nitrate can augment NO status, improve lipid homeostasis, relieve inflammation, and enhance endothelial function, suggesting that spinach is promising dietary supplements for insulin resistance prevention
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