Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.148 (Thy1)
 1,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Restriction of dietary protein is useful for chronic kidney disease (CKD) patients to protect residual renal function. However, the mechanism by which a low protein diet confers a beneficial effect in CKD patients remains unknown. One possibility is that the benefit from a low protein diet is associated with phosphorus restriction. The aim of this study is to compare the effect of protein and phosphorus on the progression of renal insufficiency using irreversible Thy1 rats, which histopathologically resemble IgA nephropathy. Irreversible Thy1 rats were fed six types of isocaloric diets consisting of three levels of protein (16.9, 12.6, and 8.4%) and two levels of phosphorus (0.5 and 0.3%) for 13 wk. Renal function was assessed biochemically and histopathologically. The low phosphorus (0.3%) diets showed protection of residual renal function regardless of dietary protein content in uremic rats. With the normal phosphorus (0.5%) diets, however, only the very low protein (8.4%) diet showed a beneficial effect, indicating that dietary phosphorus is a more important factor that affects the progression of renal insufficiency than dietary protein in this model. Furthermore, the low phosphorus diet also prevented an increase in serum parathyroid hormone, indicating that a low phosphorus diet might have beneficial effects not only for residual renal function but also for renal osteodystrophy, a typical complication of patients with CKD.
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PMID:Role of low protein and low phosphorus diet in the progression of chronic kidney disease in uremic rats. 1863 11

Phosphorus is one of the important factors that accelerate the progression of chronic kidney disease. Phosphorus restriction or phosphate binders have been reported to have the ability to prevent the progression of chronic kidney disease. FGF23 is a circulating factor that regulates renal phosphorus reabsorption and 1 alpha-hydroxylase activity. We focused on the phosphaturic activity of FGF23 and investigated whether a pharmacological dose of FGF23 is beneficial to the progression of renal insufficiency in uremic rats. To this end, we administered one of the mutant FGF23 expression plasmids into irreversible Thy1 rats. Chronic renal failure rats were established by intravenous injection of anti-rat CD90 (Thy1.1) monoclonal antibody to unilaterally nephrectomized Wistar rats. The rats were then intravenously injected every 2 wk with a naked DNA solution containing 10 microg of MOCK vector or a mutant FGF23 expression plasmid for 13 wk. Renal function was assessed biochemically and histopathologically. Mutant FGF23 significantly decreased serum creatinine and serum urea nitrogen. The marked glomerular sclerosis observed in uremic rats receiving the MOCK vector was ameliorated in rats treated with mutant FGF23. However, mutant FGF23 not only significantly decreased serum 1,25(OH)(2)D and calcium but also aggravated high-turnover renal osteodystrophy from extremely high levels of PTH. These results might be a result of the mechanisms of FGF23 such as phosphaturic activity and lowering the level of 1,25(OH)(2)D. In conclusion, mutant FGF23 prevented the progression of chronic renal failure by regulating serum phosphorus but aggravated renal osteodystrophy from the lowered levels of 1,25(OH)(2)D.
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PMID:Mutant FGF23 prevents the progression of chronic kidney disease but aggravates renal osteodystrophy in uremic rats. 1943 34