Osteoporotic bone disease in the pyridoxine-deficient rat |
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| Authors: | P J Benke H L Fleshood H C Pitot |
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| Affiliation: | 1. Department of Internal Medicine, Rochester, Minnesota;2. Division of Nephrology and Hypertension Mayo Clinic, Rochester, Minnesota;3. The Heart and Vascular Institute, University of Pittsburgh, Pennsylvania.;1. Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, California, USA;2. Department of Biostatistics, UCLA Fielding School of Public Health, Los Angeles, California, USA;3. Departments of Human Genetics and Biomathematics, David Geffen School of Medicine, Los Angeles, California, USA;4. Department of Preventive Medicine, Keck School of Medicine, University of Southern California, CA, USA;5. Department of Neurology, David Geffen School of Medicine, Los Angeles, California, USA |
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| Abstract: | Weanling rats develop osteoporosis on a high protein pyridoxine-deficient diet. Urinary o-phosphoethanolamine (OPE) levels are elevated in deficient animals and there is decrease in several hepatic enzymes which require pyridoxal phosphate as cofactor, including OPE phospholyase, an enzyme which degrades OPE. Serum alkaline phosphatase levels do not differ from control animals. Osteoporotic bone disease in the pyridoxine-deficient rat may be responsible in part for the growth failure in these animals, and may be related to the bone disease seen in some human metabolic disorders. |
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