Cardiorenal Involvement in Metabolic Syndrome Induced by Cola Drinking in Rats: Proinflammatory Cytokines and Impaired Antioxidative Protection

We report experimental evidence confirming renal histopathology, proinflammatory mediators, and oxidative metabolism induced by cola drinking. Male Wistar rats drankad libitumregular cola (C,n=12) or tap water (W,n=12).Measures.Body weight, nutritional data, plasma glucose, cholesterol fractions, TG, urea, creatinine, coenzyme Q10, SBP, and echocardiograms (0 mo and 6 mo). At 6 months euthanasia was performed. Kidneys were processed for histopathology and immunohistochemistry (semiquantitative). Compared with W, C rats showed (I) overweight (+8%,p<0.05), hyperglycemia (+11%,p<0.05), hypertriglyceridemia (2-fold,p<0.001), higher AIP (2-fold,p<0.01), and lower Q10level (−55%,p<0.05); (II) increased LV diastolic diameter (+9%,p<0.05) and volume (systolic +24%,p<0.05), posterior wall thinning (−8%,p<0.05), and larger cardiac output (+24%,p<0.05); (III) glomerulosclerosis (+21%,p<0.05), histopathology (+13%,p<0.05), higher tubular expression of IL-6 (7-fold,p<0.001), and TNFα(4-fold,p<0.001). (IV) Correlations were found for LV dimensions with IL-6 (74%,p<0.001) and TNFα(52%,p<0.001) and fully abolished after TG and Q10control. Chronic cola drinking induced cardiac remodeling associated with increase in proinflammatory cytokines and renal damage. Hypertriglyceridemia and oxidative stress were key factors. Hypertriglyceridemic lipotoxicity in the context of defective antioxidant/anti-inflammatory protection due to low Q10level might play a key role in cardiorenal disorder induced by chronic cola drinking in rats.

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A Role for Both V1a and V2 Receptors in Renal Heat Stress Injury Amplified by Rehydration with Fructose

International Journal of Molecular Sciences ◽

10.3390/ijms20225764 ◽

2019 ◽

Vol 20 (22) ◽

pp. 5764

Author(s):

Fernando E. García-Arroyo ◽

Itzel Muñoz-Jiménez ◽

Guillermo Gonzaga ◽

Edilia Tapia ◽

Horacio Osorio-Alonso ◽

...

Keyword(s):

Oxidative Stress ◽

Heat Stress ◽

Renal Damage ◽

Tap Water ◽

Renin Angiotensin System ◽

Stress Injury ◽

Mild Heat ◽

Beneficial Effects ◽

Vasopressin Receptors ◽

Male Wistar Rats

Chronic vasopressin secretion induced by recurrent mild heat stress exposure is significantly enhanced by limited rehydration with a fructose-containing beverage both in rodents and in humans. Moreover, this effect has been associated with upregulation of the polyol–fructokinase pathway and increased renal oxidative stress. Previously, we have shown that pharmacological inhibition of both V1a and V2 vasopressin receptors with conivaptan improved such renal alterations. The aim of this study was to evaluate the independent contributions of V1a and V2 receptors to the renal damage caused by mild heat stress and limited rehydration with a fructose-containing beverage. Osmotic minipumps were used to deliver either relcovaptan (0.64 mg/day) or tolvaptan (0.25 mg/day) in male Wistar rats for two weeks. Corresponding dilution vehicles were used as controls. To induce dehydration, rats were exposed to mild heat stress (37 °C for 1 h, Monday to Friday). All groups received a 10% fructose solution as a rehydration fluid for 2 h after mild heat stress. For the remainder of the day and on weekends, rats received tap water. The independent blockade of either the V1a or the V2 receptor prevented renal damage, reduced oxidative stress, and decreased plasma cortisol and systemic inflammation. However, the beneficial effects were regulated by different mechanisms. Tolvaptan inhibited polyol–fructokinase pathway overactivation, while relcovaptan prevented upregulation of the renin–angiotensin system and SGK1 expression. These data suggest that both V1a and V2 receptors participate in renal damage caused by heat stress-induced dehydration when fructose-containing beverages are used as rehydration fluids.

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Structural and functional renal alterations in five-sixth nephrectomized rats on unrestricted diet

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010014333x ◽

1986 ◽

Vol 44 ◽

pp. 342-343

Author(s):

I. Stachura ◽

M. Pardo ◽

J. Costello ◽

D.M. Landwehr

Keyword(s):

Wistar Rats ◽

Renal Damage ◽

Standard Diet ◽

Experimental Conditions ◽

Phosphate Intake ◽

Dietary Restrictions ◽

Severe Reduction ◽

Male Wistar Rats ◽

Unrestricted Diet ◽

Progressive Renal Insufficiency

Under experimental conditions severe reduction of renal mass results in the hyperfiltration of the remaining nephrons leading to a progressive renal insufficiency. Similar changes are observed in patients with various renal disorders associated with a loss of the functioning nephrons. The progression of renal damage is accelerated by high protein and phosphate intake, and may be modified by the dietary restrictions.We studied 50 five-sixth nephrectarrized male Wistar rats on a standard diet (Rodent Laboratory Chow 5001 Ralston Purina Co., Richmond, Indiana; containing 23.4% protein) over a 20 week period.

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Association between Neonatal Intakes and Hyperglycemia, and Left Heart and Aortic Dimensions at 6.5 Years of Age in Children Born Extremely Preterm

Journal of Clinical Medicine ◽

10.3390/jcm10122554 ◽

2021 ◽

Vol 10 (12) ◽

pp. 2554

Author(s):

Jawwad Hamayun ◽

Lilly-Ann Mohlkert ◽

Elisabeth Stoltz Sjöström ◽

Magnus Domellöf ◽

Mikael Norman ◽

...

Keyword(s):

Interventricular Septum ◽

Posterior Wall ◽

Root Diameter ◽

Left Ventricular ◽

Left Heart ◽

Extremely Preterm ◽

Extremely Preterm Infants ◽

Nutritional Data ◽

Aortic Dimensions

Survivors of extremely preterm birth (gestational age < 27 weeks) have been reported to exhibit an altered cardiovascular phenotype in childhood. The mechanisms are unknown. We investigated associations between postnatal nutritional intakes and hyperglycemia, and left heart and aortic dimensions in children born extremely preterm. Postnatal nutritional data and echocardiographic dimensions at 6.5 years of age were extracted from a sub-cohort of the Extremely Preterm Infants in Sweden Study (EXPRESS; children born extremely preterm between 2004–2007, n = 171, mean (SD) birth weight = 784 (165) grams). Associations between macronutrient intakes or number of days with hyperglycemia (blood glucose > 8 mmol/L) in the neonatal period (exposure) and left heart and aortic dimensions at follow-up (outcome) were investigated. Neonatal protein intake was not associated with the outcomes, whereas higher lipid intake was significantly associated with larger aortic root diameter (B = 0.040, p = 0.009). Higher neonatal carbohydrate intake was associated with smaller aorta annulus diameter (B = −0.016, p = 0.008). Longer exposure to neonatal hyperglycemia was associated with increased thickness of the left ventricular posterior wall (B = 0.004, p = 0.008) and interventricular septum (B = 0.004, p = 0.010). The findings in this study indicate that postnatal nutrition and hyperglycemia may play a role in some but not all long-lasting developmental adaptations of the cardiovascular system in children born extremely preterm.

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Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells

AJP Renal Physiology ◽

10.1152/ajprenal.00199.2002 ◽

2002 ◽

Vol 283 (5) ◽

pp. F1132-F1141 ◽

Cited By ~ 69

Author(s):

Violeta Alvarez ◽

Yasmir Quiroz ◽

Mayerly Nava ◽

Héctor Pons ◽

Bernardo Rodríguez-Iturbe

Keyword(s):

Interstitial Nephritis ◽

Renal Damage ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Malondialdehyde Content ◽

Induced Hypertension ◽

Salt Sensitive Hypertension ◽

And Control ◽

And Oxidative Stress

Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 ± 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg · kg−1 · day−1) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect of the high-salt diet (SBP = 129 ± 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.

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Dietary Choline Deprivation Exacerbates Cardiomyopathy in Streptozotocin-Induced Diabetic Adult Rats

Diabetology ◽

10.3390/diabetology2040017 ◽

2021 ◽

Vol 2 (4) ◽

pp. 190-204

Author(s):

Ahmed Al-Humadi ◽

Athina Strilakou ◽

Hussam Al-Humadi ◽

Rafal Al-Saigh ◽

Emmanouel Agapitos ◽

...

Keyword(s):

Wistar Rats ◽

Dietary Intervention ◽

Myocardial Dysfunction ◽

Posterior Wall ◽

Diabetic Rats ◽

Diabetic Rat ◽

Myocardial Inflammation ◽

Standard Diet ◽

Adult Rats ◽

Male Wistar Rats

Choline (Ch) is an essential molecule of substantial importance for the optimal development and function of several biological systems. Ch deprivation has been linked with abnormal fat metabolism, insulin resistance, and myocardial dysfunction. The current study provides evidence of an exacerbation of streptozotocin-induced cardiomyopathy in adult diabetic Wistar rats by dietary Ch deprivation through the administration of a Ch-deprived diet (CDD). Twenty-four adult male Wistar rats were randomly separated into four groups: control, diabetic (DM), choline-deprived through choline-deprived diet (CD), and diabetic choline-deprived (DM + CD). After five weeks of dietary intervention, myocardium echocardiographic and histological assessments were performed. Choline-deprived diabetic rats exhibited significantly slower heart rate, significantly higher myocardial ejection velocity and left ventricle wall tension index with a concomitant significant decreased LV posterior wall thickness as compared to diabetic rats fed on a standard diet. Moreover, histopathological evidence demonstrated an exacerbation of myocardial inflammation and fibrosis associated with significant up-regulation of VEGF expression in the diabetic rat myocardium as a result of Ch deprivation. The study’s findings are of particular significance since the examined experimental approach introduces a previously uncharacterised comorbidity simulation with regards to myocardial structure and functional profiling.

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HO-1 induction attenuates renal damage and oxidative stress induced by K2Cr2O7

Free Radical Biology and Medicine ◽

10.1016/s0891-5849(03)00068-6 ◽

2003 ◽

Vol 34 (11) ◽

pp. 1390-1398 ◽

Cited By ~ 54

Author(s):

Diana Barrera ◽

Perla D. Maldonado ◽

Omar N. Medina-Campos ◽

Rogelio Hernández-Pando ◽

María E. Ibarra-Rubio ◽

...

Keyword(s):

Oxidative Stress ◽

Renal Damage ◽

And Oxidative Stress

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Protective effects of glycyrrhizin on sub-chronic diazinon-induced biochemical, hematological alterations and oxidative stress indices in male Wistar rats

Drug and Chemical Toxicology ◽

10.1080/01480545.2018.1497053 ◽

2018 ◽

Vol 42 (3) ◽

pp. 300-308 ◽

Cited By ~ 7

Author(s):

Asieh Karimani ◽

Mohammad Heidarpour ◽

Amir Moghaddam Jafari

Keyword(s):

Oxidative Stress ◽

Wistar Rats ◽

Protective Effects ◽

Stress Indices ◽

Male Wistar Rats ◽

Hematological Alterations ◽

And Oxidative Stress

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Effect of miRNAs, proinflammatory cytokines and ACE2 in COVID-19 pathophysiology

Coronaviruses ◽

10.2174/2666796702666210303114330 ◽

2021 ◽

Vol 02 ◽

Author(s):

Hari Om Singh ◽

Kamini Jakhar ◽

Vijay Nema ◽

Asha Krishnaraj ◽

Ranjana Choudhari

Keyword(s):

Proinflammatory Cytokines ◽

Target Genes ◽

Rapid Identification ◽

Host Factors ◽

Angiotensin Converting Enzyme 2 ◽

Proinflammatory Mediator ◽

Proinflammatory Mediators ◽

Heart Blood ◽

The Difference

Background: Angiotensin converting enzyme 2 (ACE2) is the main cellular receptor for entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and acts as a proinflammatory mediator of Coronavirus disease (COVID-19). The clinical outcome of SARS-CoV-2 infection is influenced by proinflammatory mediators. The specific microRNAs (miRNAs) influence the ACE2 expression and are accountable for the increased circulatory proinflammatory mediator levels. Thus host factors play a crucial role in COVID-19 pathophysiology. The pathogenesis of COVID-19 disease is not well understood. Hence we comprehended the role of miRNAs, proinflammatory cytokines and ACE2 in COVID-19 pathophysiology. Methods: We utilized multiple databases, specifically, EMBASE, PubMed (Medline) and Google Scholar for our search. Discussion: SARS-CoV-2 genes could be target of host miRNAs. The miRNAs regulate the expression of ACE2 in various organs including kidney, heart, blood vessels, and lung. ACE2 acts as a proinflammatory mediator of SARS-CoV-2 associated disease. Proinflammatory cytokines (IL-6, IL-1β and TNF) have been associated with severe COVID-19 disease. Hence variation in expression of miRNAs would influence the regulation of COVID-19 pathophysiology. The clinical outcomes of COVID -19 are variable which could be linked with the difference in binding of host miRNA to target genes. Conclusion: Correlation of these genes with severe or critical stages of patients will provide biomarkers for severity of lung inflammation which would be useful in rapid identification of patients in need of hospital admission. Analysis of relationship between the miRNAs and ACE2 will be helpful in designing anti-miR therapy for ACE2-related SARS-CoV-2 infection.

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