Abstract
The effects of dietary protein and fat on renal function‐related blood and urine parameters, such as excretion of urinary protein and inflammatory cytokines, were investigated in adriamycin (ADR)‐induced nephrotic syndrome rats.ADR (2 mg/kg BW) was injected i.p. weekly for six weeks to induce nephrotic syndrome. Rats were fed low‐ (C:P:F = 53:7:40, LPHF) or high‐protein (C:P:F = 63:30:7, HPLF) diets for five weeksAt the end of the experiment, Serum albumin, TG and creatinine levels were significantly higher in the LPHF group than in the HPLF group although serum total cholesterol levels did not differ between the two groups. BUN and UUN levels were lower in the LPHF group than in the HPLF group. Protein and creatintine excretion in the urine was significantly higher in the HPLF group than in the LPHF group. Serum inflammatory cytokine levels did not differ between the two groups. Levels of IL‐6, TNF‐α, and IL‐13 in splenocyte supernatants were significantly higher in the LPHF group than in the HPLF group.We confirmed that dietary protein and fat might affect blood and urine parameters, including protein excretion in urine and splenocyte inflammatory cytokine levels in ADR‐induced nephrotic syndrome rats.
Highlights
Nephrotic syndrome (NS) is a general symptom of renal disease and is associated with abnormal immune response [1,2,3]
This study was conducted to investigate the effects of dietary protein and fat contents on renal function and inflammatory cytokine levels in rats with nephrotic syndrome
We could observe that serum albumin levels decreased and serum lipid levels increased, as well as urinary protein increased
Summary
Nephrotic syndrome (NS) is a general symptom of renal disease and is associated with abnormal immune response [1,2,3]. Nephrotic syndrome shows symptoms of hypoalbuminemia, hyperlipidemia, and proteinuria. It has been reported that dietary protein and fat affect the symptoms of nephrotic syndrome. Chronic degenerative diseases such as hyperlipidemia, hypertension, atherosclerosis, and diabetes mellitus promote renal function decline. Animal study showed that hyperlipidemia could damage renal vascular endothelial cells and cause glomerular interstitial cell proliferation by increasing platelet aggregation and platelet-derived growth factor levels [4]. Glomerular interstitial cell proliferation increases low-density lipoprotein cholesterol (LDL-chol) and free radical generation [5]
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