Effect of Prolonged Uremia on Insulin-Like Growth Factor-I Receptor Autophosphorylation and Tyrosine Kinase Activity in Kidney and Muscle
| Autor: | Michael M. Friedlaender, Ralph Rabkin, Tanny Tsao, Yu Chen, Fernando C. Fervenza |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Male
medicine.medical_specialty Physiology medicine.medical_treatment Kidney urologic and male genital diseases Receptor IGF Type 1 Rats Sprague-Dawley Insulin-like growth factor Internal medicine Genetics medicine Animals Insulin-Like Growth Factor I Phosphorylation Kinase activity Muscle Skeletal Receptor Uremia business.industry Body Weight Autophosphorylation General Medicine Acute Kidney Injury Protein-Tyrosine Kinases medicine.disease Rats Endocrinology medicine.anatomical_structure Solubility Nephrology Creatinine Kidney Failure Chronic Signal transduction business Tyrosine kinase Signal Transduction |
| Zdroj: | Nephron Experimental Nephrology. 10:285-292 |
| ISSN: | 1660-2129 |
| DOI: | 10.1159/000063703 |
| Popis: | Recently, based on a study in rats with chronic renal failure (CRF), it has been suggested that IGF-I resistance in uremia may be caused in part by defective IGF-I receptor autophosphorylation and tyrosine kinase activity. Thus if such a defect were to develop in prolonged acute renal failure (ARF), this may explain why IGF-I therapy, effective in rats, has failed to promote recovery from ARF in patients. Accordingly, we examined IGF-I receptor function in rats with uremia of increasing duration and in pair-fed sham-operated controls. After 6 days of prolonged ARF, kidney IGF-I receptor binding increased twofold, while IGF-I stimulated receptor phosphorylation and tyrosine kinase activity were unchanged. Muscle receptor binding, autophosphorylation and tyrosin kinase activity were similar to control values after 6 or even 21 days of uremia. Taking all these findings together it appears that IGF-I resistance in uremia cannot be attributed to a receptor defect. This in turn argues against altered receptor function as a cause of the failure of IGF-I to modify clinical ARF. |
| Databáze: | OpenAIRE |
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