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Other reported mechanisms may also apply for tubular damage in ArgII knock out mice 65, 66. To that purpose, it would be interesting to determine in future studies, whether l -cit supplementation to ArgII knock out mice prevents diabetes-induced tubular damage and enhancement of BUN levels. Intriguingly, collagen deposition in kidneys isolated from diabetic ArgII knock out mice was not different from the one observed in control WT mice. A limited availability of the precursor proline, provided by the ArgII ornithine aminotransferase pathway, may be the cause of reduced renal collagen synthesis crosslink in this group, which indicates that ArgII has an important contribution to renal collagen content. However, the cost-effect of specific ArgII inhibition in advanced stages of diabetic animal models remains to be investigated, clenbuterol cycle supplements.
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