BES2003 Oral Communications Cardiovascular Endocrinology (8 abstracts)
Characterisation of the metabolic syndrome in the stroke prone spontaneously hypertensive rat and the contribution of the Y chromosome
P Strahorn 1 , D Graham 1 , B Champange 1 , FJ Charchar 1 , L Crawford 2 , N Sattar 2 & AF Dominiczak 1
1Division of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK; 2Department of Clinical Biochemistry, University of Glasgow, Royal Infirmary, Glasgow, UK.
Objective: The spontaneously hypertensive stroke prone rat (SHRSP) is a model of insulin resistance and dyslipidemia. Feeding a 60% fructose diet exaggerates these phenotypes. The Y chromosome may influence lipid levels in the spontaneously hypertensive rat (SHR). Therefore we aim to characterise the metabolic syndrome using in vivo and dyslipidemic phenotpyes in the SHRSP and examine the contribution of the Y chromosome.
Methods: SHRSP and WKY Y consomic strains (SP.WKYGlaYw and WKY.SPGlaYs) were constructed. At 10 weeks of age SHRSP (n=8), WKY (n=8) and the reciprocal Y consomic strains (n=8) were fed either normal diet or a 60% fructose diet for 14 days. Tail cuff blood pressure (SBP) measurements were taken before and after fructose feeding. At 12 weeks of age an intraperitoneal glucose tolerance test (IPGTT) was performed after an overnight fast. At sacrifice lipid profile including plasma triglycerides (TG), total cholesterol (chol), HDL cholesterol NEFA and insulin was measured.
Results: SBP (mmHg) was significantly higher in SHRSP 181±4.1***, and WKY.SPGlaYs 163+9.8* when compared to WKY 142±6.7. TGs (mmol/L) were significantly lower in WKY 1.7±0.2***, and SP.WKYGlaYw 4.65±0.5* when compared to SHRSP 4.1±0.5. Significant differences between SHRSP and WKY were observed for Chol (mmol/L) 2.6±0.1 vs 1.6±0.1***, HDL (mmol/L) 2.24±0.04 vs 1.3±0.02***, NEFA (mmol/L) 2.6±0.1 vs 2.3±0.1*, Insulin 0.45±0.11 vs 0.31±0.12 and IPGTT (AUC) 30.5±1.3 vs 22.7±2.3* respectively. The Y chromosome had no effect on plasma lipids or IPGTT. *p<0.05, **p<0.01, ***p<0.001.
Conclusion: The fructose fed SHRSP may be considered as a model of the human metabolic syndrome. Furthermore, the Y chromosome may contribute to abnormalities in lipid metabolism and hypertension in the SHRSP.
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Endocrine Abstracts
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