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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
Main Authors: Py, Guillaume, Eydoux, Nicolas, Perez-Martin, Antonia, Raynaud, Eric, Brun, Jean-Frédéric, Préfaut, Christian, Mercier, Jacques
Format: Article
Language:English
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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.
ISSN:0026-0495
1532-8600
DOI:10.1053/meta.2001.21692