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Phosphorus intake regulates intestinal function and polyamine metabolism in uremia
Y Imanishi1, H Koyama, M Inaba
1Department of Biochemistry, Osaka City University Medical School, Japan.
Kidney International
|February 1, 1996
Summary
Uremic rats develop secondary hyperparathyroidism and intestinal dysfunction due to low vitamin D levels. Phosphorus restriction and vitamin D treatment improve these conditions by restoring polyamine metabolism and intestinal cell function.
Area of Science:
- Nephrology
- Endocrinology
- Gastroenterology
Background:
- Chronic kidney disease (CKD) leads to secondary hyperparathyroidism and altered vitamin D metabolism.
- Uremia is associated with intestinal dysfunction, including changes in polyamine metabolism and cell proliferation.
- The role of 1,25-dihydroxyvitamin D deficiency in uremia-induced intestinal issues is not fully understood.
Purpose of the Study:
- To investigate the impact of uremia on intestinal polyamine metabolism and cell proliferation in rats.
- To examine the role of 1,25-dihydroxyvitamin D deficiency in uremia-induced intestinal dysfunction.
- To assess the effects of phosphorus restriction and vitamin D supplementation on these parameters.
Main Methods:
- Induction of uremia in rats via 5/6-nephrectomy.
- Measurement of serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels.
- Assessment of intestinal calcium absorption, calbindin-D9k gene expression, and polyamine metabolism (ODC, spermidine/spermine N1-acetyltransferase).
- Analysis of c-fos and c-jun gene expression in the intestine.
- Intervention with phosphorus restriction and 1,25-dihydroxyvitamin D3 injection.
Main Results:
- Uremic rats exhibited secondary hyperparathyroidism, decreased serum 1,25-(OH)2D, reduced calcium absorption, and altered intestinal gene expression (decreased calbindin-D9k, increased ODC, c-fos, c-jun).
- Phosphorus restriction partially reversed these changes, increasing serum 1,25-(OH)2D and improving intestinal parameters.
- 1,25-dihydroxyvitamin D3 administration normalized calbindin-D9k mRNA and reduced ODC, c-fos, and c-jun mRNA levels, indicating its protective role.
Conclusions:
- 1,25-dihydroxyvitamin D deficiency is a key factor in uremia-induced intestinal dysfunction and villus proliferation.
- Altered polyamine metabolism, driven by 1,25-dihydroxyvitamin D deficiency, contributes significantly to intestinal pathology in uremia.
- Phosphorus restriction and vitamin D repletion show therapeutic potential for managing intestinal complications in CKD.