Abstract
Fructose, an everyday component of western diet associated to chronic hyperglycemia and enhanced free radical production, impairs endothelial function and supplementation with antioxidants might improve it. In this study we investigated if vitamin E could reverse the microvascular damage elicited by fructose. Male Syrian golden hamsters drank either 10% fructose solution (F) or filtered water (C), combined with three concentrations of vitamin E in their chows [zero, normal (VE) or 5X (5XVE)] during 60 days. Microvascular reactivity in response to topical application of acetylcholine (Ach; endothelium-dependent vasodilator) or sodium nitroprusside (SNP; endothelium-independent vasodilator) and macromolecular permeability increase induced by either 30 min ischemia followed by reperfusion (I/R) or topical application of histamine (5 μM) were assessed using the cheek pouch preparation. Compared to controls (drinking filtered water), fructose-drinking animals showed decreased vasodilatation to acetylcholine in all concentrations tested (-56.2% for 10-9M, -53.9% for 10-7M and -43.7% for 10-5M). On the other hand, vitamin E supplementation resulted in increased responses for both water and fructose drinking groups (177.4% for F vs. F/5XVE and 241.6% for C vs. C/5XVE for 10-5M Ach). Endothelial-independent vasodilatation explored by topical application of SNP was restored and even enhanced with the supplementation of 5X vitamin E in both groups (80.1% for F vs. F/5XVE; 144.2% for C vs. C/5XVE; 3.4% of difference for C/5XVE vs. F/5XVE on 10-5M SNP). The number of leaky sites after I/R and histamine stimuli in vitamin E supplemented animals decreased (-25.1% and -15.3% for F vs. F/5XVE; and -21.7% and -16% of leaky sites comparing C vs. C/5XVE, respectively for I/R and histamine stimuli) pointing to tightening of the endothelial barrier for macromolecular permeability. Our results strongly suggest that vitamin E could improve the endothelial function and permeability barrier and also reverse impairments elicited by sugar overload.
Highlights
Humans present a tendency to choose more palatable diets and sugars like fructose and glucose function as daily sweeteners
The average fructose intake was 4 mg/kg/day and the caloric intake did not differ between animals, but those drinking 10% fructose solution showed a trend towards lower consumption (Table 2)
In our investigation it was possible to demonstrate that substitution of the drinking water by 10% fructose solution, in hamsters, elicited hyperglycemia, hyperinsulinemia, endothelial dysfunction and increased microvascular permeability for macromolecules
Summary
Humans present a tendency to choose more palatable diets and sugars like fructose and glucose function as daily sweeteners. The scenario of prolonged hyperglycemia is associated to permanent damage, dysfunction and failure of various tissues and organs, including kidneys, nerves and retina [1,2,3] These clusters of abnormalities are associated to higher incidence of cardiovascular morbidity and mortality. Fructose ingestion can cause insulin resistance, hyperglycemia, and hypertriglyceridemia in rats [9] These animals display different abnormalities, such as reduction in tritiated glucose uptake by adipocytes, reduction of endothelium-dependent vasodilatation induced by acetylcholine in aortic strips [10], reduction to 80% in tyrosine phosphorylation of IRS-1 in the soleus muscle [11], increase in fasting plasma insulin without hyperglycemia, decreased muscarinic receptors expression, increased dependence on nitric oxide (NO) and impairment of α2adrenergic-mediated relaxation [12]. If our hypothesis is correct, the use of this particular vitamin, as daily supplement, might function as future therapeutic approach to prevent microangiopathies
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