Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats.
@article{SnchezLozada2007FructoseinducedMS,
title={Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats.},
author={Laura Gabriela S{\'a}nchez-Lozada and Edilia Tapia and Adriana Jim{\'e}nez and Pablo Bautista and Magdalena Crist{\'o}bal and Tom{\'a}s Nepomuceno and Virgilia Soto and Carmen {\'A}vila-Casado and Takahiko Nakagawa and Richard J. Johnson and Jaime Herrera-Acosta and Martha Franco},
journal={American journal of physiology. Renal physiology},
year={2007},
volume={292 1},
pages={
F423-9
}
}Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, the metabolic syndrome has been epidemiologically linked with renal progression. The renal hemodynamic effects of fructose intake are unknown, as well as the effects of different routes of administration. Metabolic syndrome was induced in rats over 8 wk by either a high-fructose diet (60%, F60, n = 7) or by adding fructose to drinking water (10%, F10, n = 7). Body weight and food and fluid intake of…
316 Citations
Manifestations of Renal Impairment in Fructose-induced Metabolic Syndrome
- MedicineCureus
- 2017
Under the conditions of a fructose-induced metabolic syndrome, high serum UA and CRP correlate to the development of early renal disorders without a clinical manifestation of renal dysfunction.
Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome.
- Medicine, BiologyAmerican journal of physiology. Renal physiology
- 2008
Normalization of plasma UA with Fx in rats with metabolic syndrome alleviated both metabolic and glomerular hemodynamic and morphological alterations, providing further evidence for a pathogenic role of hyperuricemia in fructose-mediated metabolic syndrome.
Synergistic effect of uricase blockade plus physiological amounts of fructose-glucose on glomerular hypertension and oxidative stress in rats.
- Biology, MedicineAmerican journal of physiology. Renal physiology
- 2013
Findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose.
Effects of Fructose-Induced Metabolic Syndrome on Kidney Histology in Rats
- Biology, Medicine
- 2020
It is demonstrated that metabolic syndrome may adversely affect kidney histology and cause renal damage.
Diet-induced hypertension in rats is associated with increased renal vasoconstrictor response to angiotensin II after imitated endothelial dysfunction.
- Medicine, BiologyMicrovascular research
- 2022
Ursodeoxycholic Acid Ameliorates Fructose-Induced Metabolic Syndrome in Rats
- Biology, MedicinePloS one
- 2014
Treatment with UDCA successfully ameliorated the deleterious effects of fructose and might support possible clinical application of UDCA in MS patients especially those present with liver diseases, taking into account its tolerability and safety.
Fructose, but not dextrose, accelerates the progression of chronic kidney disease.
- MedicineAmerican journal of physiology. Renal physiology
- 2007
Testing the hypothesis that consumption of a high-fructose diet could accelerate the progression of chronic kidney disease in the rat remnant kidney model concluded that this risk factor for kidney disease is high.
The fructose-fed rat: a review on the mechanisms of fructose-induced insulin resistance and hypertension
- Biology, MedicineMolecular and Cellular Biochemistry
- 2009
The role of sympathetic nervous system overactivation, increased production of vasoconstrictors, such as endothelin-1 and angiotensin II, and prostanoids in the development of hypertension in fructose-fed rats is addressed.
Intra-Renal Angiotensin Levels Are Increased in High-Fructose Fed Rats in the Extracorporeal Renal Perfusion Model
- Biology, MedicineFront. Physiol.
- 2018
Results suggest that rats fed high fructose affect renal RAS, which may contribute to several deleterious effects of fructose on the kidneys and consequently an increase in blood pressure.
The Establishment of Metabolic Syndrome Model by Induction of Fructose Drinking Water in Male Wistar Rats
- Medicine, BiologyBioMed research international
- 2014
The metabolic syndrome rat model is best established with the induction of FDW 20% for eight weeks, which was evident in the form of higher obesity parameter which caused the development of the metabolic syndrome.
References
SHOWING 1-10 OF 44 REFERENCES
A causal role for uric acid in fructose-induced metabolic syndrome.
- Medicine, BiologyAmerican journal of physiology. Renal physiology
- 2006
The first evidence that uric acid may be a cause of metabolic syndrome is provided, possibly due to its ability to inhibit endothelial function, as well as a reduced vasodilatory response of aortic artery rings to acetylcholine.
Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome
- Medicine, BiologyNature Clinical Practice Nephrology
- 2005
Fructose-induced hyperuricemia results in endothelial dysfunction and insulin resistance, and might be a novel causal mechanism of the metabolic syndrome.
Fructose-induced insulin resistance and hypertension in rats.
- Medicine, BiologyHypertension
- 1987
The addition of clonidine to the drinking water inhibited fructose-induced hypertension, but not the increase in plasma insulin or triglyceride concentration seen in fructose-fed rats, indicating that the metabolic changes associated with fructose- induced hypertension are unlikely to be secondary to an increase in sympathetic activity.
Fructose-induced hypertension in rats is concentration- and duration-dependent.
- MedicineJournal of pharmacological and toxicological methods
- 1995
Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats.
- Medicine, BiologyKidney international
- 2005
These studies provide a potential mechanism by which hyperuricemia can mediate hypertension and renal disease and partially prevented arteriolopathy and glomerular hypertension associated with significantly less infiltration of CD5+ cells.
Hyperuricemia Causes Glomerular Hypertrophy in the Rat
- Medicine, BiologyAmerican Journal of Nephrology
- 2002
Hyperuricemic rats develop glomerular hypertrophy that can be prevented in part by ACE inhibitor therapy, and prolonged hyperuricemia is associated with the development of glomerulosclerosis in the rat.
Fructose, weight gain, and the insulin resistance syndrome.
- MedicineThe American journal of clinical nutrition
- 2002
Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietaryructose in humans.
Reversal of fructose-induced hypertension and insulin resistance by chronic losartan treatment is independent of AT2 receptor activation in rats
- Medicine, BiologyJournal of hypertension
- 2005
It is suggested that reversal of high fructose-induced hypertension and insulin resistance by chronic losartan treatment is not dependent on AT2R activation and that functional activation of AT1R plays a major role in the pathogenesis ofhigh fructose- induced hypertension and diabetes resistance.
Mild hyperuricemia induces glomerular hypertension in normal rats.
- Medicine, BiologyAmerican journal of physiology. Renal physiology
- 2002
Mildly hyperuricemic rats develop renin-dependent hypertension and interstitial renal disease. Hyperuricemia might also induce changes in glomerular hemodynamics. Micropuncture experiments under deep…
Evidence for a Causal Role of the Renin-Angiotensin System in Vascular Dysfunction Associated With Insulin Resistance
- BiologyHypertension
- 2004
The novel observation of insulin Resistance-induced upregulation of AT1 receptor expression could explain the association of insulin resistance with endothelial dysfunction and hypertension.



