Location

CSU Ballroom

Start Date

21-4-2014 10:00 AM

End Date

21-4-2014 11:30 AM

Student's Major

Chemistry and Geology

Student's College

Science, Engineering and Technology

Mentor's Name

Theresa Salerno

Mentor's Email Address

theresa.salerno@mnsu.edu

Mentor's Department

Chemistry and Geology

Mentor's College

Science, Engineering and Technology

Description

Normal abundant dietary sugars such as fructose and glucose can contribute to hypertension and other health issues. To avoid these health complications, many individuals use artificial sweeteners. An equivalent intake of some artificial sweeteners also can lead to hypertension. However, Stevia, a sweetener that is isolated from a Paraguayan plant, was shown in relevant literature to decrease blood pressure in both rat specimens and humans. The general purpose of this research project was to study the effect of Stevia and glucose on the expression of two key components of the renin-angiotensin-aldosterone system (RAAS): prorenin receptor (PRR) and angiotensin receptor type 1 (AT1). Increased expression of renin and angiotensin can lead to vasoconstriction and systemic hypertension. Their effects are mediated by their binding to PRR and AT1. Therefore, decreases in the expression of these receptor proteins can result in lowered blood pressure. Rats were fed diets supplemented with glucose, saccharin, or Stevia over a six-week period and the kidneys were obtained. qPCR designs were developed to measure the relative amounts of PRR receptor and AT1 receptor. The methods had efficiencies greater than 97% and gave reproducible results. Then the developed methods were used to measure the expression of AT1 and PRR in the different rat kidney samples. Preliminary results with a small sample group suggest that glucose might cause an increase in the expression of both AT1 and PRR compared to the standard diet. Further experimentation will also document the effects of short-term exposure to Stevia in the diet.

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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Apr 21st, 10:00 AM Apr 21st, 11:30 AM

Effect of Artificial Sweeteners on the Renin-Angiotensin System in Rats

CSU Ballroom

Normal abundant dietary sugars such as fructose and glucose can contribute to hypertension and other health issues. To avoid these health complications, many individuals use artificial sweeteners. An equivalent intake of some artificial sweeteners also can lead to hypertension. However, Stevia, a sweetener that is isolated from a Paraguayan plant, was shown in relevant literature to decrease blood pressure in both rat specimens and humans. The general purpose of this research project was to study the effect of Stevia and glucose on the expression of two key components of the renin-angiotensin-aldosterone system (RAAS): prorenin receptor (PRR) and angiotensin receptor type 1 (AT1). Increased expression of renin and angiotensin can lead to vasoconstriction and systemic hypertension. Their effects are mediated by their binding to PRR and AT1. Therefore, decreases in the expression of these receptor proteins can result in lowered blood pressure. Rats were fed diets supplemented with glucose, saccharin, or Stevia over a six-week period and the kidneys were obtained. qPCR designs were developed to measure the relative amounts of PRR receptor and AT1 receptor. The methods had efficiencies greater than 97% and gave reproducible results. Then the developed methods were used to measure the expression of AT1 and PRR in the different rat kidney samples. Preliminary results with a small sample group suggest that glucose might cause an increase in the expression of both AT1 and PRR compared to the standard diet. Further experimentation will also document the effects of short-term exposure to Stevia in the diet.

Recommended Citation

Ball, Jacob. "Effect of Artificial Sweeteners on the Renin-Angiotensin System in Rats." Undergraduate Research Symposium, Mankato, MN, April 21, 2014.
http://cornerstone.lib.mnsu.edu/urs/2014/poster_session_A/33

 

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