In Sprague Dawley rats with insulin resistance induced by fructose 10% in the drinking water, how long does it take to observe a significant increase in blood pressure from baseline?
If you are using a tail cuff method to measure blood pressure, be sure to fully habituate the rats to the procedure before starting your intervention. If you run a placebo group, you will see drops in blood pressure for the first two weeks due to habituation to the tail cuff procedure.
Administration of 10% fructose in drinking water should significantly increase SBP after week 2 and will continue to increase for the next 2 weeks reaching a plateau by week 4-5. Coadministration of a high-salt diet accelerates the process and should take about a week to observe an increase in SBP.
If you are using a tail cuff method to measure blood pressure, be sure to fully habituate the rats to the procedure before starting your intervention. If you run a placebo group, you will see drops in blood pressure for the first two weeks due to habituation to the tail cuff procedure.
My own experience is that, measuring with an sphingomanometer, you will need at least 2-3 months to detect a significant increase in BP. This was done in female rats, I do not know whether males behave similarly or not.
Yes. Our cell culture studies have shown that insulin increases endothelin-1 (ET-1) production (Kidney Int 2000; 57: 2492-2501).
ET-1 is a potent vasoconstrictor and can increase blood pressure (BP). High glucose also increases ET-1 production. Thus a dual effect of diabetes with or without insulin resistance in increasing BP exists. However, it should be noted that osmotic diuresis and volume loss caused by uncontrolled diabetes often offset the potential for BP rise.
My view is that it may take at least several months for you to detect a significant increase in systolic blood pressure in Sprague Dawley rats with insulin resistance induced by fructose 10% in the drinking water. It is quite difficult to induce insulin resistance and/or type 2 diabetes in SD rats or C57BL/6J mice by oral glucose administration, because the animals have normal pancreatic alpha and beta function to adequately regulate blood glucose metabolism.
5 years ago, we published an article in Clin Sci (Lond). 2008 May;114(9):591-601, entitled "Long-term hyperglucagonaemia induces early metabolic and renal phenotypes of Type 2 diabetes in mice". Please see the data shown in Table 2 or 3? We did not observe any significant effects on blood pressure, glucose tolerance and tissue injury in C57BL/6J mice fed 2% glucose in driniking water continuously for 4 weeks. We could't believe the data, so we fed C57BL/6J mice with 5% glucose continuously for more than 3 months. We did not publish the data because the findings clearly go against main stream diabetic research. The effects were only minimal and still not significant and we had to give up. However, the only caveats are that we did not use 10% fructose as you use, and that we have not tested this in other mouse models which may have genetic and functional phenotypes of increased insulin resistance and type 2 diabetes.