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Original Article

Korean J Physiol Pharmacol 2020; 24(4): 319-328

Published online July 1, 2020

Copyright © Korean J Physiol Pharmacol.

Activation of the renin-angiotensin system in high fructose-induced metabolic syndrome

Mina Kim1,2,3, Ga Young Do1, and Inkyeom Kim1,2,3,*

1Department of Pharmacology, 2Cardiovascular Research Institute, 3Department of Biomedical Science, School of Medicine, Kyungpook National University, Daegu 41944, Korea

Correspondence to:Inkyeom Kim

Received: February 5, 2020; Revised: May 19, 2020; Accepted: May 21, 2020

This is an Open Access journal distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague?Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

Keywords: Fructose, Hypertension, Metabolic syndrome, Obesity, Renin-angiotensin system