title: Diet-induced endothelial dysfunction in the rat is independent of the degree of increase in total body weight.
abstract: A growing number of studies indicate an association between obesity, insulin resistance, dyslipidaemia and cardiovascular disorders, collectively known 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 diet, and examined its effects on metabolic changes and vascular reactivity of Wistar rats. At the end of the experiment, the cafeteria-diet fed group was divided into two groups of low weight gain (LWG) and high weight gain (HWG). Both LWG and HWG groups had significantly (P<0.01) higher fat-pad mass than their chow-fed counterparts, while gastrocnemius muscle mass were comparable. All cafeteria-diet fed rats had significantly (P<0.01) raised plasma triacylglycerol (TG) levels whereas plasma non-esterified fatty acids, glucose and insulin levels were similar between chow-fed and cafeteria-diet fed rats. Vasorelaxation responses to acteylcholine, insulin and sodium nitroprusside were significantly (P<0.01) attenuated in cafeteria-diet fed animals; however, there were no differences in contractile responses of the mesenteric arteries to noradrenaline or KCl between the groups. Multiple regression analysis showed a significant (P<0.05) negative association between plasma TG levels and reduction in acetylcholine-induced vasorelaxation. Acetylcholine-induced vasorelaxation was also significantly (P<0.05) associated with the amount of fat-pad mass. These data suggest that diet-induced vascular dysfunction can occur in the absence of insulin resistance, and that plasma TGs may have a detrimental effect on vascular reactivity.
authors.affiliation: Diabetes and Endocrinology Research Unit, Department of Medicine, University of Liverpool, UCD, Daulby Street, Liverpool L693GA, UK. naderali@liverpool.ac.uk
authors.forename: E K
authors.initials: EK
authors.lastname: Naderali
authors.forename: L C
authors.initials: LC
authors.lastname: Pickavance
authors.forename: J P
authors.initials: JP
authors.lastname: Wilding
authors.forename: G
authors.initials: G
authors.lastname: Williams
mesh_terms: D000818:Animals; D004032:Diet / Q000009:adverse effects*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D007328:Insulin / Q000494:pharmacology; D017566:Microvascular Angina / Q000503:physiopathology*; D009765:Obesity / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D015430:Weight Gain / Q000502:physiology
chemical_list: D007328:Insulin; D014280:Triglycerides