scholarly journals High-Fat Diet-Induced Renal Proximal Tubular Inflammatory Injury: Emerging Risk Factor of Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Shuxian Chen ◽  
Jinxia Chen ◽  
Shangmei Li ◽  
Fengbiao Guo ◽  
Aifen Li ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Risk Factor ◽  
Kidney Disease ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
High Fat ◽  
Inflammatory Injury ◽  
Emerging Risk ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

Nowadays, with the improvements in living standards and changes in living habits, high-fat diet (HFD) has become much more common in the populations worldwide. Recent studies have shown that HFD could induce lipid accumulation, and structural and functional abnormalities, accompanied by the release of large amounts of pro-inflammatory cytokines, in proximal tubular epithelial cells (PTECs). These findings indicate that, as an emerging risk factor, PTEC injury-induced by HFD may be closely related to inflammation; however, the potential mechanisms underlying this phenomenon is still not well-known, but may involve the several inflammatory pathways, including oxidative stress-related signaling pathways, mitochondrial dysfunction, the myeloid differentiation factor 2/Toll like receptor 4 (MD2/TLR4) signaling pathway, the ERK1/2-kidney injury molecule 1 (KIM-1)-related pathway, and nuclear factor-κB (NF-κB) activation, etc., and the detailed molecular mechanisms underlying these pathways still need further investigated in the future. Based on lipid abnormalities-induced inflammation is closely related to the development and progression of chronic kidney disease (CKD), to summarize the potential mechanisms underlying HFD-induced renal proximal tubular inflammatory injury, may provide novel approaches for CKD treatment.

scholarly journals Delayed Exercise Training Improves Obesity-Induced Chronic Kidney Disease by Activating AMPK Pathway in High-Fat Diet-Fed Mice

2020 ◽  
Vol 22 (1) ◽  
pp. 350
Author(s):  
Florian Juszczak ◽  
Maud Vlassembrouck ◽  
Olivia Botton ◽  
Thomas Zwakhals ◽  
Morgane Decarnoncle ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Exercise Training ◽  
High Fat Diet ◽  
Interstitial Fibrosis ◽  
Calorie Intake ◽  
Acid Oxidation ◽  
Obese Mice ◽  
High Fat ◽  
Ampk Pathway

Exercise training is now recognized as an interesting therapeutic strategy in managing obesity and its related disorders. However, there is still a lack of knowledge about its impact on obesity-induced chronic kidney disease (CKD). Here, we investigated the effects of a delayed protocol of endurance exercise training (EET) as well as the underlying mechanism in obese mice presenting CKD. Mice fed a high-fat diet (HFD) or a low-fat diet (LFD) for 12 weeks were subsequently submitted to an 8-weeks EET protocol. Delayed treatment with EET in obese mice prevented body weight gain associated with a reduced calorie intake. EET intervention counteracted obesity-related disorders including glucose intolerance, insulin resistance, dyslipidaemia and hepatic steatosis. Moreover, our data demonstrated for the first time the beneficial effects of EET on obesity-induced CKD as evidenced by an improvement of obesity-related glomerulopathy, tubulo-interstitial fibrosis, inflammation and oxidative stress. EET also prevented renal lipid depositions in the proximal tubule. These results were associated with an improvement of the AMPK pathway by EET in renal tissue. AMPK-mediated phosphorylation of ACC and ULK-1 were particularly enhanced leading to increased fatty acid oxidation and autophagy improvement with EET in obese mice.

scholarly journals Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
María M. Adeva-Andany ◽  
Carlos Fernández-Fernández ◽  
David Mouriño-Bayolo ◽  
Elvira Castro-Quintela ◽  
Alberto Domínguez-Montero
Keyword(s):  
Chronic Kidney Disease ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Sodium Bicarbonate ◽  
Negative Impact ◽  
Qtc Interval ◽  
Bicarbonate Therapy ◽  
Proximal Tubular ◽  
Acute Metabolic Acidosis ◽  
Renal Proximal Tubular

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Lack of adiponectin in mice accelerates high-fat diet-induced progression of chronic kidney disease

Life Sciences ◽  
2020 ◽  
Vol 257 ◽  
pp. 118061
Author(s):  
Beatriz M.V. Pereira ◽  
Karina Thieme ◽  
Larissa de Araújo ◽  
Alice C. Rodrigues
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
High Fat Diet ◽  
High Fat

scholarly journals High-Fat Diet Induced Hedgehog Signaling Modifications during Chronic Kidney Damage

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Rabia Mehmood ◽  
Nadeem Sheikh ◽  
Muhammad Babar Khawar ◽  
Muddasir Hassan Abbasi ◽  
Asima Tayyeb ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
High Fat Diet ◽  
Hedgehog Signaling ◽  
Body Weight Gain ◽  
Organ Damage ◽  
Dietary Fats ◽  
Control Group ◽  
High Fat ◽  
Adult Rats

Excessive consumption of dietary fats leads to the deposition of unnecessary metabolites and multiple organ damage. Lipids, important key regulators of Hedgehog signaling, are involved in triggering fibrotic chronic kidney disease. The present study encompasses the assessment of renal morphofunctional modifications and alteration of lipid metabolism influencing the changes in gene expression of hedgehog signaling pathway genes. Fifteen male Rattus norvegicus of 200 ± 25 grams weight were equally divided into three groups: control (standard rat chow), D-1 (unsaturated high-fat diet) and D-2 (saturated high-fat diet). Animals were provided with respective diets and were followed for 16 weeks. Both HFD-fed groups did not show overall body weight gain as compared to the control. While significant downregulation of hedgehog pathway genes was found in fatty diet groups. In comparison with the control group, Shh, Gli1, Gli2, and Gli3 were downregulated after the consumption of both unsaturated and saturated fatty diets. Ihh and Smo exhibit a similar downregulation in the D-1 group, but an upregulation was detected in the D-2 group. D-2 group also had an increased serum urea concentration as compared to the control ( P = 0.0023 ). Furthermore, renal histopathology revealed tubular necrosis, glomerular edema, glomerular shrinkage, and hypocellularity. Collagen deposition in both HFD groups marks the extent of fibrosis summary figure. Extravagant intake of dietary fats impaired normal kidney functioning and morphofunctionally anomalous kidney triggers on Hh signaling in adult rats. These anomalies can be linked to an escalated risk of chronic kidney disease in adults strongly recommending the reduced uptake of fatty diets to prevent impaired metabolism and renal lipotoxicity.

Effects of honey supplementation on renal dysfunction and metabolic acidosis in rats with high-fat diet-induced chronic kidney disease

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Omotayo O. Erejuwa ◽  
Daniel Ogbonna John Aja ◽  
Nkemjika I. Uwaezuoke ◽  
Kenneth I. Nwadike ◽  
Basil Chukwuma Ezeokpo ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Drinking Water ◽  
Renal Function ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Total Calcium ◽  
High Fat

AbstractBackgroundMetabolic diseases are associated with impaired renal function which accelerates chronic kidney disease (CKD) progression. The aim of this study was to investigate the effects of 16-week honey supplementation on renal function, metabolic acidosis and renal abnormalities in Wistar rats fed a high-fat diet (HFD).MethodsWistar rats were fed a HFD and sucrose (30%) solution and randomly grouped and treated. Group 1 was fed rat chow and treated with drinking water while groups 2, 3, 4 and 5 were fed a HFD and treated with drinking water, 1, 2 and 3 g/kg body weight (BW) of honey, respectively, once daily for 16 weeks. After the rats were sacrificed, the serum samples were obtained and used for the analysis of total cholesterol, urea, creatinine, sodium, potassium, calcium, bicarbonates and chloride ions. Histopathological examinations of the kidneys were performed.ResultsThe serum creatinine and anion gap levels were significantly (p < 0.01) higher while the levels of serum total calcium and ionized fraction were significantly (p < 0.01) lower in HFD-fed control rats than in chow-fed rats. The kidney of HFD-fed control rats was characterized by tubular necrosis, glomerular atrophy, hemorrhage and severe focal aggregate inflammatory (FAIC) cells. Honey treatment (1, 2 or 3 g/kg BW) prevented elevations in serum creatinine while it restored serum levels of total calcium and ionized calcium towards those in rats fed chow only. All the three doses of honey also significantly (p < 0.01) reduced anion gap and ameliorated renal lesions. Honey treatment (2 g/kg BW) significantly (p < 0.05) increased bicarbonate and chloride ion in HFD-fed rats compared with HFD-fed control rats.ConclusionsSixteen-week honey supplementation ameliorates renal dysfunction, metabolic acidosis and renal morphological abnormalities in HFD-fed Wistar rats.

Abstract 14859: IL17 Contribute to the Atherosclerotic Development and the Initiation of Chronic Kidney Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yusuke Tanigaito ◽  
Kayoko Sato ◽  
Kazutaka Kitamura ◽  
Atsuko Futase ◽  
Keiko Fukushima ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
T Cells ◽  
Kidney Disease ◽  
High Fat Diet ◽  
Inflammatory Cytokine ◽  
Urinary Albumin ◽  
Creatinine Ratio ◽  
High Fat ◽  
Albumin Creatinine Ratio ◽  
Deficient Mice

Introduction: Recent studies suggested that the atherogenic state correlated with progression of chronic kidney disease (CKD). However, it is not known whether sustained status of chronic inflammation in atherosclerosis is closely linked to the development of CKD. Hypothesis: Inflammatory cytokine producing-T cells in the advanced atherosclerosis induced the dysfunction of podocytes. Methods/Results: Eighteen-week-old apolipoprotein E-deficient mice (Control) were fed with high-fat diet for 8W (ApoE) and compared to IL17/ApoE-double deficient mice fed with high-fat diet (DKO). Sudan staining of aorta revealed the atherosclerotic lesion was increased in ApoE compared to Control, and inhibited in DKO. Activated IFNγ + CD4 T cells (Th1) and IL17 + CD4 T cells (Th17) were significantly increased in ApoE compared to DKO by FACS. Immunohistochemistry of aortic sinus showed many Th1 and Th17 were infiltrated in the atherosclerotic plaque in ApoE, however, inflammatory infiltrates were inhibited in DKO. Furthermore, the urinary albumin/creatinine ratio was increased significantly in ApoE compared to DKO. Th1 and Th17 were correlated with the urinary albumin/creatinine ratio, and many Th1 and Th17 were observed in the glomeruli. Next, to investigate whether the inflammatory cytokine induced dysfunction of podocytes were involved in proteinuria, we investigated nephrin, podocin, and phosphorylated nephrin in the kidney by Western blots and immunohistochemistry. The decreased phosphorylated neprin in ApoE were recovered in DKO. Finally, we confirmed that the morphological changed of podocytes in ApoE were improved in DKO by electron microscopy. Conclusion: Recruitments of IFNγ + Th1 and IL17 + Th17 T cells might aggravate atherosclerosis acceleration and induce the initiation of glomerular tissue damage.

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