ArticlePeerJ2017
The metabolic profile of a rat model of chronic kidney disease.
Article in PeerJ, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The role of redox signaling in mitochondria and endoplasmic reticulum regulation in kidney diseases.Archives of toxicology · 2025Review
- Label-free whole-kidney metabolic optical imaging usingBiomedical optics express · 2025Article
- Canagliflozin attenuates kidney injury, gut-derived toxins, and gut microbiota imbalance in high-salt diet-fed Dahl salt-sensitive rats.Renal failure · 2024Article
- Nephrectomy and high-salt diet inducing pulmonary hypertension and kidney damage by increasing Ang II concentration in rats.Respiratory research · 2024Article
- DNA methylation of miR-181a-5p mediated by DNMT3b drives renal interstitial fibrosis developed from acute kidney injury.Epigenomics · 2024Article
- Effects of Exercise Training on Mitochondrial Fatty Acid β-Oxidation in the Kidneys of Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- Metabolic Responses of Normal Rat Kidneys to a High Salt Intake.Function (Oxford, England) · 2023Article
- Impact of high salt diets on CHOP-mediated apoptosis and renal fibrosis in a rat model.Molecular biology reports · 2021Article
- Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases.Biomolecules · 2021Review
- L-phenylalanine attenuates high salt-induced hypertension in Dahl SS rats through activation of GCH1-BH4.PloS one · 2021Article
- The physiological and molecular mechanisms to maintain water and salt homeostasis in response to high salt intake in Mongolian gerbils (Meriones unguiculatus).Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2020Article
- Nitric oxide and oxidative stress pathways do not contribute to sex differences in renal injury and function in Dahl SS/Jr rats.Physiological reports · 2020Article
- Analysis of Cardiac Metabolic Remodeling in Heart Failure Using Nuclear Medicine and Its Application: Japanese Society of Nuclear Cardiology Award.Annals of nuclear cardiology · 2020Review
- Gene Expression Studies and Targeted Metabolomics Reveal Disturbed Serine, Methionine, and Tyrosine Metabolism in Early Hypertensive Nephrosclerosis.Kidney international reports · 2019Article
- Ameliorative effects of hydrogen sulfide (NaHS) on chronic kidney disease-induced brain dysfunction in rats: implication on role of nitric oxide (NO) signaling.Metabolic brain disease · 2018Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe kidney is always subjected to high metabolic demand. The aim of this study was to characterize metabolic profiles of a rat model of chronic kidney disease (CKD) with cardiorenal syndrome (CRS) induced by prolonged hypertension.
methodsWe used inbred male Dahl salt-sensitive (DS) rats fed an 8% NaCl diet from six weeks of age (high-salt; HS group) or a 0.3% NaCl diet as controls (low-salt; LS group). We analyzed function, pathology, metabolome, and the gene expression related to energy metabolism of the kidney.
resultsDS rats with a high-salt diet showed hypertension at 11 weeks of age and elevated serum levels of creatinine and blood urea nitrogen with heart failure at 21 weeks of age. The fibrotic area in the kidneys increased at 21 weeks of age. In addition, gene expression related to mitochondrial function was largely decreased. The levels of citrate and isocitrate increased and the gene expression of alpha-ketoglutaratedehydrogenase and succinyl-CoA synthetase decreased; these are enzymes that metabolize citrate and isocitrate, respectively. In addition, the levels of succinate and acetyl Co-A, both of which are metabolites of the tricarboxylic acid (TCA) cycle, decreased.
conclusionsDS rats fed a high-salt diet were deemed a suitable model of CKD with CRS. Gene expression and metabolites related to energy metabolism and mitochondria in the kidney significantly changed in DS rats with hypertension in accordance with the progression of renal injury.
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