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Streptozotocin-induced diabetes decreases rat sarcolemmal lactate transport
Impaired lactate metabolism is a metabolic disorder, which is not fully understood in the diabetic state including streptozotocin (STZ)-induced diabetes. We investigated whether STZ-induced diabetes results in altered lactate exchanges using the rat muscle sarcolemmal vesicles (SV) model. Fifteen da...
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Published in: | Metabolism, clinical and experimental clinical and experimental, 2001-04, Vol.50 (4), p.418-424 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Impaired lactate metabolism is a metabolic disorder, which is not fully understood in the diabetic state including streptozotocin (STZ)-induced diabetes. We investigated whether STZ-induced diabetes results in altered lactate exchanges using the rat muscle sarcolemmal vesicles (SV) model. Fifteen days after diabetes onset (1 STZ-injection, 65 mg/kg, intraperitoneal [IP]), rats had higher blood and muscle lactate concentrations compared with normal rats (1.50 ± 0.09 v 1.95 ± 0.21 mmol/L (not significant [NS]) and 21.02 ± 1.26 v 25.53 ± 0.98 mmol/kg wet weight (ww); P < .05). The initial rate of lactate uptake was measured at various external lactate concentrations using SV of both group in zero-trans conditions. STZ-induced diabetes decreased the initial rate of total lactate influx at external lactate concentrations from 1 to 100 mmol/L (P < .05). This decrease in lactate transport was found in addition to an increased free radical production, as indicated by a significant increase in malonedialdehyde (MDA) concentration (64.3 ± 8.7 v 100.3 ± 13.5 nmol · g−1 ww, P < .05), coupled with a higher glutathione peroxidase (Gpx) activity (48.03 ± 3.13 v 84.7 ± 15.01 μmol · min−1 · mg−1 protein, P < .05) in red gastrocnemius. We concluded that STZ-induced diabetes decreases total lactate transport activity in rat SV and is associated with increased muscular oxidative stress. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1053/meta.2001.21692 |