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Am J Physiol Endocrinol Metab 281: E1308-E1315, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 6, E1308-E1315, December 2001

Impaired sarcolemmal vesicle lactate uptake and skeletal muscle MCT1 and MCT4 expression in obese Zucker rats

Guillaume Py1, Karen Lambert1, Antonia Perez-Martin1, Eric Raynaud2, Christian Préfaut1, and Jacques Mercier1

2 Département de Physiologie, Laboratoire de Physiologie des Interactions, Institut de Biologie, and 1 Département de Biochimie Métabolique et Clinique, Faculté de Pharmacie, 34060 Montpellier, France

The present experiments were undertaken to characterize 1) the hindlimb muscle mass lactate uptake and 2) the expression of monocarboxylate transporter isoforms MCT1 and MCT4, as well as lactate dehydrogenase (LDH) isozyme distribution, in various skeletal muscles of Zucker fa/fa rats taken as a model of insulin resistance-related obesity. Initial lactate uptake at six different concentrations was measured in sarcolemmal vesicles (SV) by use of L-[U-14C]lactate. Compared with controls, the maximal rate of lactate uptake and affinity were decreased in SV of Zucker rats (~30%) in which MCT4 content was significantly decreased (P < 0.05). MCT4 expression was decreased in soleus, extensor digitorum longus, and red tibialis anterior (RTA; P < 0.05), but not in white tibialis anterior, whereas MCT1 expression was decreased only in RTA of Zucker rats (P < 0.05). Obesity led to a shift toward type M-LDH isozyme in mixed muscles. We conclude that obesity leads to changes in muscular MCT1 and MCT4 expression, which, when associated with LDH isozyme redistribution, may contribute to the hyperlactatemia noted in insulin resistance.

monocarboxylate transporter; muscle fiber type; lactate transport; lactate dehydrogenase isozyme; Zucker fa/fa rat


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