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Am J Physiol Heart Circ Physiol (January 27, 2006). doi:10.1152/ajpheart.01002.2005
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Submitted on September 19, 2005
Accepted on January 18, 2006

Effects of high-sucrose feeding on insulin resistance and hemodynamic responses to insulin in spontaneously hypertensive rats

Sebastien Melancon1, Helene Bachelard1*, Mylene Badeau1, Frederic Bourgoin1, Maryse Pitre1, Richard Lariviere1, and Andre Nadeau1

1 Department of Medicine and Lipid Research Unit, Laval University, Ste-Foy, Quebec, Canada

* To whom correspondence should be addressed. E-mail: helene.bachelard{at}crchul.ulaval.ca.

This study was designed to investigate the effects of a sucrose diet on vascular and metabolic actions of insulin in spontaneously hypertensive rats (SHR). Male SHR were randomized to receive a sucrose- or regular chow-diet for 4 weeks. Age-matched chow-fed WKY rats were used as normotensive control. In a first series of experiments, the three groups of rats had pulsed Doppler flow probes and intravascular catheters implanted to determine blood pressure, heart rate and blood flows. Insulin sensitivity was assessed during a euglycemic hyperinsulinemic clamp performed in conscious rats. In a second series of experiments, new groups of rats were used to examine glucose transport activity in isolated muscles, and to determine endothelial nitric oxide synthase (eNOS) protein expression in muscles, and endothelin content in vascular tissues. Sucrose feeding was shown to markedly enhance the pressor response to insulin, and its hindquarter vasoconstrictor effect, when compared to chow-fed SHR. A reduction in eNOS protein content in muscle, but no change in vascular ET-1 protein were noted in sucrose-fed SHR when compared to WKY rats, but these changes were not different from those noted in chow-fed SHR. Similar reductions in insulin-stimulated glucose transport were observed in soleus muscles from both groups of SHR, when compared with WKY rats. In extensor digitorum longus muscles a significant reduction in insulin-stimulated glucose transport was only seen in sucrose-fed rats, when compared with the other two groups. Environmental factors, that is high intake of simple sugars, could possibly potentiate the genetic predisposition in SHR to endothelial dysfunction and insulin resistance.




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