A high-fat, high-fructose diet induced hepatic steatosis, renal lesions, dyslipidemia, and hyperuricemia in non-obese rats DOI Creative Commons
Ika Yustisia,

Delvina Tandiari,

Muhammad Husni Cangara

et al.

Heliyon, Journal Year: 2022, Volume and Issue: 8(10), P. e10896 - e10896

Published: Oct. 1, 2022

Excessive consumption of fat and sugar is associated with various chronic diseases. However, the variation content in diet greatly affected outcome. In this study, a high-fat, high-fructose (HFHFD) formula was made composition 31.99% carbohydrate, 40.7% fat, 11.8% protein, an additional 30% fructose drink to confirm effects HFHFD on metabolic health pathological changes organs, especially liver, kidneys, pancreas, muscles, spleen. A total 24 male Wistar rats aged 8-12 weeks were divided into four groups: standard chow (SC), HFHFD, SC + carbon tetrachloride (CCl4), CCl4. After eight dietary intervention, body mass index, obesity lipid profiles, liver function tests, fasting blood glucose, serum uric acid urea levels, tissue histopathology examined. main unsaturated fatty acids linoleic (14.57%) palmitoleic (8.28%), saturated stearic (13.62%) myristic (10.09%), low trans-fatty content, did not promote become obese. histology examination showed severe hepatic steatosis (78.33%), leading steatohepatitis accompanied by increase ALP (p < 0.01), triglyceride 0.001), cholesterol 0.05), 0.001) levels. Other histological features moderate lesions (45%) kidney, slight vacuolization mild inflammatory cells spleen muscle. So, study found that although within 8 administration, it induced renal lesions, dyslipidemia, hyperuricemia as consequence excessive fructose.

Language: Английский

Obesity and chronic kidney disease DOI

Zongmiao Jiang,

Yao Wang, Xue Zhao

et al.

AJP Endocrinology and Metabolism, Journal Year: 2022, Volume and Issue: 324(1), P. E24 - E41

Published: Nov. 16, 2022

The prevalence of obesity has increased dramatically during the past decades, which been a major health problem. Since 1975, number people with worldwide nearly tripled. An increasing studies find as driver chronic kidney disease (CKD) progression, and mechanisms are complex include hemodynamic changes, inflammation, oxidative stress, activation renin-angiotensin-aldosterone system (RAAS). Obesity-related is characterized by glomerulomegaly, often accompanied localized segmental glomerulosclerosis lesions. In these patients, early symptoms atypical, microproteinuria being main clinical manifestation nephrotic syndrome rare. Weight loss RAAS blockers have protective effect on obesity-related CKD, but even so, significant proportion patients eventually progress to end-stage renal despite treatment. Thus, it critical comprehend underlying CKD create new tactics for slowing or stopping progression. this review, we summarize current knowledge disease, its pathological future perspectives

Language: Английский

Citations

152
Oxidative stress and inflammation in diabetic nephropathy: role of polyphenols DOI Creative Commons
Qi Jin, Tong‐Tong Liu, Yuan Qiao

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: July 21, 2023

Diabetic nephropathy (DN) often leads to end-stage renal disease. Oxidative stress demonstrates a crucial act in the onset and progression of DN, which triggers various pathological processes while promoting activation inflammation forming vicious oxidative stress-inflammation cycle that induces podocyte injury, extracellular matrix accumulation, glomerulosclerosis, epithelial-mesenchymal transition, tubular atrophy, proteinuria. Conventional treatments for DN have limited efficacy. Polyphenols, as antioxidants, are widely used with multiple targets fewer adverse effects. This review reveals stress-associated led damage cells, including podocytes, endothelial mesangial epithelial cells. It potent antioxidant anti-inflammatory properties by targeting Nrf2, SIRT1, HMGB1, NF-κB, NLRP3 polyphenols, quercetin, resveratrol, curcumin, phenolic acid. However, there remains long way comprehensive understanding molecular mechanisms applications clinical therapy polyphenols.

Language: Английский

Citations

140
Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease DOI Creative Commons
Hsin‐Jung Ho, Hitoshi Shirakawa

Cells, Journal Year: 2022, Volume and Issue: 12(1), P. 88 - 88

Published: Dec. 25, 2022

The kidney contains many mitochondria that generate ATP to provide energy for cellular processes. Oxidative stress injury can be caused by impaired with excessive levels of reactive oxygen species. Accumulating evidence has indicated a relationship between oxidative and diseases, revealed new insights into mitochondria-targeted therapeutics renal injury. Improving mitochondrial homeostasis, increasing biogenesis, balancing turnover the potential protect function against stress. Although there are some reviews addressed this issue, articles summarizing effects risk factors failure still few. In review, we integrate recent studies on in especially chronic disease. We organized causes kidneys based their effects. This review also listed possible candidates clinical diseases modulating function.

Language: Английский

Citations

115
Oxidative stress: The nexus of obesity and cognitive dysfunction in diabetes DOI Creative Commons
Huimin Li, Jing Ren, Yusi Li

et al.

Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 14

Published: April 3, 2023

Obesity has been associated with oxidative stress. Obese patients are at increased risk for diabetic cognitive dysfunction, indicating a pathological link between obesity, stress, and dysfunction. can induce the biological process of stress by disrupting adipose microenvironment (adipocytes, macrophages), mediating low-grade chronic inflammation, mitochondrial dysfunction (mitochondrial division, fusion). Furthermore, be implicated in insulin resistance, inflammation neural tissues, lipid metabolism disorders, affecting diabetics.

Language: Английский

Citations

66
Exposure to different surface-modified polystyrene nanoparticles caused anxiety, depression, and social deficit in mice via damaging mitochondria in neurons DOI
Yuhan Ma, Dihui Xu,

Zicheng Wan

et al.

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 919, P. 170739 - 170739

Published: Feb. 9, 2024

Language: Английский

Citations

23
Protective Role of Vitamin D Receptor Against Mitochondrial Calcium Overload from PM2.5-Induced Injury in Renal Tubular Cells DOI Creative Commons

Mengqiu Lu,

Zishun Zhan,

Dan Li

et al.

Redox Biology, Journal Year: 2025, Volume and Issue: unknown, P. 103518 - 103518

Published: Jan. 1, 2025

Language: Английский

Citations

2
Anthocyanins from the fruits ofLycium ruthenicumMurray improve high-fat diet-induced insulin resistance by ameliorating inflammation and oxidative stress in mice DOI
Baoming Tian, Jianhua Zhao, Xiaoqing Xie

et al.

Food & Function, Journal Year: 2021, Volume and Issue: 12(9), P. 3855 - 3871

Published: Jan. 1, 2021

Anthocyanins from the fruits ofLycium ruthenicumMurray improve high-fat diet-induced insulin resistance by ameliorating inflammation and oxidative stress in mice.

Language: Английский

Citations

64
Programmed Cell Death in Diabetic Nephropathy: A Review of Apoptosis, Autophagy, and Necroptosis DOI
Nour S. Erekat

Medical Science Monitor, Journal Year: 2022, Volume and Issue: 28

Published: Aug. 10, 2022

Diabetic nephropathy is a common complication of type I and II diabetes, in which renal glomeruli are destroyed, resulting damage, proteinuria, hypertension. Apoptosis, autophagy, necroptosis 3 forms programmed cell death that have been implicated the pathogenesis diabetic nephropathy. Apoptosis podocytes leads to glomerular injury podocyte depletion, associated with proteinuria structural damage Additionally, epithelial cells proximal convoluted tubules also undergo apoptosis nephropathy, leading tubular atrophy, causes depletion subsequent formation atubular association loss function. On other hand, insufficiency autophagy has correlated For instance, decreased autophagic activity shown kidney, causing variations function disruption filtration barrier. Furthermore, attenuated demonstrated buildup impaired molecules organelles, normally broken down by proteinuria. Moreover, might key role decline Thus, this article aims review mechanisms effects including roles apoptosis, necroptosis.

Language: Английский

Citations

64
Kidney Damage Caused by Obesity and Its Feasible Treatment Drugs DOI Open Access
Meihui Wang, Zixu Wang, Yaoxing Chen

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(2), P. 747 - 747

Published: Jan. 11, 2022

The rapid growth of obesity worldwide has made it a major health problem, while the dramatic increase in prevalence had significant impact on magnitude chronic kidney disease (CKD), especially developing countries. A vast amount researchers have reported strong relationship between and disease, can serve as an independent risk factor for disease. histological changes kidneys obesity-induced renal injury include glomerular or tubular hypertrophy, focal segmental glomerulosclerosis bulbous sclerosis. Furthermore, inflammation, hemodynamic changes, insulin resistance lipid metabolism disorders are all involved development progression nephropathy. However, there is no targeted treatment obesity-related In this review, RAS inhibitors, SGLT2 inhibitors melatonin would be presented to treat injury. we concluded that protect damage caused by inhibiting inflammation oxidative stress, revealing its therapeutic potential.

Language: Английский

Citations

54
Placental Mesenchymal Stem Cells Alleviate Podocyte Injury in Diabetic Kidney Disease by Modulating Mitophagy via the SIRT1-PGC-1alpha-TFAM Pathway DOI Open Access

Xiudan Han,

Jiao Wang,

Ruilin Li

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(5), P. 4696 - 4696

Published: Feb. 28, 2023

The use of mesenchymal stem cells (MSCs) has become a new strategy for treating diabetic kidney disease (DKD). However, the role placenta derived (P-MSCs) in DKD remains unclear. This study aims to investigate therapeutic application and molecular mechanism P-MSCs on from perspective podocyte injury PINK1/Parkin-mediated mitophagy at animal, cellular, levels. Western blotting, reverse transcription polymerase chain reaction, immunofluorescence, immunohistochemistry were used detect expression injury-related markers mitophagy-related markers, SIRT1, PGC-1α, TFAM. Knockdown, overexpression, rescue experiments performed verify underlying DKD. Mitochondrial function was detected by flow cytometry. structure autophagosomes mitochondria observed electron microscopy. Furthermore, we constructed streptozotocin-induced rat model injected into rats. Results showed that as compared with control group, exposing podocytes high-glucose conditions aggravated injury, represented decreased Podocin along increased Desmin, inhibited mitophagy, manifested Beclin1, LC3II/LC3I ratio, Parkin, PINK1 associated an P62. Importantly, these indicators reversed P-MSCs. In addition, protected mitochondria. mitochondrial membrane potential ATP content accumulation reactive oxygen species. Mechanistically, alleviated inhibition enhancing SIRT1-PGC-1α-TFAM pathway. Finally, results revealed largely related significantly TFAM group. conclusion, ameliorated activating

Language: Английский

Citations

31