Diet-induced endothelial dysfunction in the rat is independent of the degree of increase in total body weight

Citation
Ek. Naderali et al., Diet-induced endothelial dysfunction in the rat is independent of the degree of increase in total body weight, CLIN SCI, 100(6), 2001, pp. 635-641
Citations number
41
Categorie Soggetti
Medical Research General Topics
Journal title
CLINICAL SCIENCE
ISSN journal
01435221 → ACNP
Volume
100
Issue
6
Year of publication
2001
Pages
635 - 641
Database
ISI
SICI code
0143-5221(200106)100:6<635:DEDITR>2.0.ZU;2-M
Abstract
A growing number of studies indicate an association between obesity, insuli n resistance, dyslipidaemia and cardiovascular disorders. collectively know n as Syndrome X. In this study we have aimed to produce a model of Syndrome X by voluntary feeding of Wistar rats with a highly palatable cafeteria di et, and examined its effects on metabolic changes and vascular reactivity o f Wistar rats. At the end of the experiment, the cafeteria-diet fed group w as divided into two groups of low weight gain (LWG) and high weight gain (H WG). Both LWG and HWG groups had significantly (P < 0.01) higher fat-pad ma ss than their chow-fed counterparts, while gastrocnemius muscle mass were c omparable. All cafeteria-diet fed rats had significantly (P < 0.01) raised plasma triacylglycerol (TG) levels whereas plasma non-esterified fatty acid s, glucose and insulin levels were similar between chow-fed and cafeteria-d iet fed rats. Vasorelaxation responses to acteylcholine, insulin and sodium nitroprusside were significantly (P < 0.01) attenuated in cafeteria-diet f ed animals; however, there were no differences in contractile responses of the mesenteric arteries to noradrenaline or KCI between the groups. Multipl e regression analysis showed a significant (P < 0.05) negative association between plasma TG levels and reduction in acetylcholine-induced vasorelaxat ion. Acetylcholine-induced vasorelaxation was also significantly (P < 0.05) associated with the amount of fat-pad mass. These data suggest that diet-i nduced vascular dysfunction can occur in the absence of insulin resistance, and that plasma TGs may have a detrimental effect on vascular reactivity.