T1R2 and T1R3 Knockouts in a Mouse Model Showed Significant Attenuation of Fuctose-Induced, Salt-Sensitive Hypertension
Eaton, Andrew J.
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The increasing amount of fructose used in the Western diet and increased fructose consumption result in metabolic syndrome, obesity, and hypertension. The specific cellular mechanisms leading to these ailments are highly debated. One of these mechanisms involves taste receptors that send signals to the body to direct fructose absorption. To determine the significance of the T1R family of gene products and their role in development of hypertension through a high fructose, high salt diet, we hypothesized that KO T1R2/3 mice would not develop the hypertension associated with prolonged diets of high fructose and high salt when treated with this diet. Recent data has discovered a significant increase in blood pressure leading to hypertension when rodents are treated with 20% fructose over 1-2 weeks, and 20% fructose/4% NaCl diets over 4-6 weeks. To determine the effects ofT1R2/3, we ran two protocols: one based on a short-term, high fructose diet, and the other based around a long-term high fructose and high salt diet in order to induce hypertension. Using t-tests to compare systolic blood pressures before and after diet treatment, we discovered a significance attenuation of systolic blood pressure in the KO T1R2/3 group from the control. These data supports the idea that T1R2 and T1R3 could be involved with renal regulation of sodium absorption, excretion and homeostasis. Our results open the door to a plethora of continual research opportunities, including the relationship between fructose stimulation ofT1R2 and T1R3 gene products as they relate to NHE3, and the renin-angiotensin system.