High-fructose Diet Induces Earlier and More Severe Kidney Damage than High-fat Diet on Rats | ||||
| Egyptian Journal of Histology | ||||
| Article 18, Volume 44, Issue 2, June 2021, Page 535-544 PDF (1.03 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejh.2020.31508.1304 | ||||
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| Authors | ||||
Rasha A Elsisy 1; Mohammed Abu El-Magd  2; Mona A Abdelkarim1
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| 1Department of Anatomy, Faculty of Medicine, Kafrelsheikh University | ||||
| 2Department of Anatomy, Faculty of Veterinary Medicine, Kafrelsheikh University | ||||
| Abstract | ||||
| Background: Several previous studies explored the toxic effect of high-fat diet (HFD) and high-fructose diet (HFrD), however little is known regarding their differential detrimental effects on the kidney. Aim: This study was conducted to compare the biochemical, histological, and molecular changes in the kidney induced by consumption of HFD and HFrD for 4 and 8 weeks. Materials and Methods: Thirty-five rats were randomly divided into five groups (n = 7/group): control, HFD1 (fed HFD for 4w), HFrD1 (for 4w), HFD2 (for 8w), and HFrD2 (for 8w). The studied parameters involved kidney function markers [urea, creatinine, and retinol-binding protein (RBP)] in the serum, histological examination using H&E stains, immunohistochemical examination of alpha-smooth muscle actin (áSMA), and expression of inflammation and glomerulosclerosis-related genes [tumor necrosis alpha (TNFá), interleukin 1â (IL1â), and nuclear factor kappa B (NFêB)], and necrosis-related genes [poly(ADP-ribose) polymerase-1 (PARP1) and receptor-interacting protein (RIP1)] in the kidney using real-time PCR. Results: Earlier and more severe renal damage were noticed in rats fed HFrD than HFD-fed rats as evidenced by 1) significantly (p < 0.05) higher levels of kidney function parameters (urea, creatinine, and RBP), 2) a higher kidney histopathological score (glomerulosclerosis, glomerular necrosis, Bowman’s space dilation, coagulative necrosis, cloudy swelling, and fat droplets deposition in renal tubules, congestion and mononuclear cells infiltration in interstitium), 3) a significantly (p < 0.01) higher positive áSMA staining in renal capillaries and some tubular cells, 4) a significantly (p < 0.05) upregulated expression of (TNFá, IL1â, and NFêB), 5) a significantly (p < 0.05) increased expression of (PARP1 and RIP1). The highest damage order was noticed in HFrD2, followed by HFrD1 and then HFD2. No notable renal damage was observed in HFD1 as compared to the control group. Conclusion: The findings of this study highlight the ability of HFrD to induce earlier and more severe renal damage than HFD. | ||||
| Keywords | ||||
| Glomerulosclerosis; high-fat diet; high-fructose diet; kidney histopathological score; necrosis | ||||
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