Faculty Opinions recommendation of AMPK mediates the initiation of kidney disease induced by a high-fat diet.

2011 ◽  
Author(s):  
Mai Ots-Rosenberg
Keyword(s):  
Kidney Disease ◽  
High Fat Diet ◽  
High Fat

2038-P: Rice Endosperm Protein Intake in Childhood Suppresses the Development of High-Fat Diet-Induced Metabolic Disorders and Kidney Disease during Adulthood in Mice

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2038-P
Author(s):  
YUKI HIGUCHI ◽  
MICHIHIRO HOSOJIMA ◽  
HIDEYUKI KABASAWA ◽  
SHOJI KUWAHARA ◽  
RYOHEI KASEDA ◽  
...  
Keyword(s):  
Kidney Disease ◽  
High Fat Diet ◽  
Protein Intake ◽  
Metabolic Disorders ◽  
High Fat ◽  
Rice Endosperm ◽  
Endosperm Protein

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 AMPK Mediates the Initiation of Kidney Disease Induced by a High-Fat Diet

2011 ◽  
Vol 22 (10) ◽  
pp. 1846-1855 ◽  
Author(s):  
Anne-Emilie Declèves ◽  
Anna V. Mathew ◽  
Robyn Cunard ◽  
Kumar Sharma
Keyword(s):  
Kidney Disease ◽  
High Fat Diet ◽  
High Fat

scholarly journals Effects of high-fat diet and losartan on renal cortical blood flow using contrast ultrasound imaging

2013 ◽  
Vol 305 (9) ◽  
pp. F1343-F1351 ◽  
Author(s):  
Anne-Emilie Declèves ◽  
Joshua J. Rychak ◽  
Dan J. Smith ◽  
Kumar Sharma
Keyword(s):  
Blood Flow ◽  
Kidney Disease ◽  
Ultrasound Imaging ◽  
High Fat Diet ◽  
Microvascular Perfusion ◽  
High Fat ◽  
Cortical Blood Flow ◽  
Perfusion Time ◽  
Cortical Perfusion ◽  
Losartan Treatment

Obesity-related kidney disease occurs as a result of complex interactions between metabolic and hemodynamic effects. Changes in microvascular perfusion may play a major role in kidney disease; however, these changes are difficult to assess in vivo. Here, we used perfusion ultrasound imaging to evaluate cortical blood flow in a mouse model of high-fat diet-induced kidney disease. C57BL/6J mice were randomized to a standard diet (STD) or a high-fat diet (HFD) for 30 wk and then treated either with losartan or a placebo for an additional 6 wk. Noninvasive ultrasound perfusion imaging of the kidney was performed during infusion of a microbubble contrast agent. Blood flow within the microvasculature of the renal cortex and medulla was derived from imaging data. An increase in the time required to achieve full cortical perfusion was observed for HFD mice relative to STD. This was reversed following treatment with losartan. These data were concurrent with an increased glomerular filtration rate in HFD mice compared with STD- or HFD-losartan-treated mice. Losartan treatment also abrogated fibro-inflammatory disease, assessed by markers at the protein and messenger level. Finally, a reduction in capillary density was found in HFD mice, and this was reversed upon losartan treatment. This suggests that alterations in vascular density may be responsible for the elevated perfusion time observed by imaging. These data demonstrate that ultrasound contrast imaging is a robust and sensitive method for evaluating changes in renal microvascular perfusion and that cortical perfusion time may be a useful parameter for evaluating obesity-related renal disease.

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 Caffeic Acid Attenuates Diabetic Kidney Disease via Modulation of Autophagy in a High-Fat Diet/Streptozotocin- Induced Diabetic Rat

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Marwa Matboli ◽  
Sanaa Eissa ◽  
Doaa Ibrahim ◽  
Marwa G. A. Hegazy ◽  
Shalabia S. Imam ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Caffeic Acid ◽  
High Fat Diet ◽  
Diabetic Kidney Disease ◽  
Diabetic Rat ◽  
High Fat ◽  
Diabetic Kidney

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.

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