Abundance and subcellular distribution of MCT1 and MCT4 in heart and fast-twitch skeletal muscles

Bonen, Arend; Miskovic, Dragana; Tonouchi, Mio; Lemieux, Kathleen; Wilson, Marieangela C.; Marette, André; Halestrap, Andrew P.

doi:10.1152/ajpendo.2000.278.6.e1067

Cited by 94 publications

(154 citation statements)

References 35 publications

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“…The GLUT-4 was detected with a commercially available antibody (East Acres Biologicals). The monocarboxylate transporter MCT4 was detected by using an antibody prepared in our laboratory (7).…”

Section: Methodsmentioning

confidence: 99%

Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane

Luiken

Dyck

Han³

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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189

173

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-It is well known that muscle contraction and insulin can independently translocate GLUT-4 from an intracellular depot to the plasma membrane. Recently, we have shown that the fatty acid transporter FAT/CD36 is translocated from an intracellular depot to the plasma membrane by muscle contraction (Ͻ30 min) (Bonen et al. J Biol Chem 275: 14501-14508, 2000). In the present study, we examined whether insulin also induced the translocation of FAT/CD36 in rat skeletal muscle. In studies in perfused rat hindlimb muscles, we observed that insulin increased fatty acid uptake by ϩ51%. Insulin increased the rate of palmitate incorporation into triacylglycerols, diacylglycerols, and phospholipids (P Ͻ 0.05) while reducing muscle palmitate oxidation (P Ͻ 0.05). Perfusing rat hindlimb muscles with insulin increased plasma membrane FAT/CD36 by ϩ48% (P Ͻ 0.05), whereas concomitantly the intracellular FAT/CD36 depot was reduced by 68% (P Ͻ 0.05). These insulin-induced effects on FAT/CD36 translocation were inhibited by the phosphatidylinositol 3-kinase inhibitor LY-294002. Thus these studies have shown for the first time that insulin can induce the translocation of FAT/CD36 from an intracellular depot to the plasma membrane.This reveals a previously unknown level of regulation of fatty acid transport by insulin and may well have important consequences in furthering our understanding of the relation between fatty acid metabolism and insulin resistance.

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Section: Methodsmentioning

confidence: 99%

Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane

Luiken

Dyck

Han³

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

Self Cite

189

173

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“…FAT/CD36 and FABPpm protein content was determined in both homogenates and giant sarcolemmal vesicles prepared from heart, skeletal muscle, adipose tissue, and liver ( Fig. 1), as we have described previously (6,8,9,11,29). For detection of FAT/CD36 and FABPpm, we used MO-25 (30) and a rabbit polyclonal anti-FABPpm antiserum (13), respectively.…”

Section: Northern and Western Blottingmentioning

confidence: 98%

Changes in fatty acid transport and transporters are related to the severity of insulin deficiency

Luiken

Arumugam

Bell

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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106

119

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We have examined the effects of streptozotocin (STZ)-induced diabetes (moderate and severe) on fatty acid transport and fatty acid transporter (FAT/CD36) and plasma membrane-bound fatty acid binding protein (FABPpm) expression, at the mRNA and protein level, as well as their plasmalemmal localization. These studies have shown that, with STZ-induced diabetes, 1) fatty acid transport across the plasma membrane is increased in heart, skeletal muscle, and adipose tissue and is reduced in liver; 2) changes in fatty acid transport are generally not associated with changes in fatty acid transporter mRNAs, except in the heart; 3) increases in fatty acid transport in heart and skeletal muscle occurred with concomitant increases in plasma membrane FAT/CD36, whereas in contrast, the increase and decrease in fatty acid transport in adipose tissue and liver, respectively, were accompanied by concomitant increments and reductions in plasma membrane FABPpm; and finally, 4) the increases in plasma membrane transporters (FAT/CD36 in heart and skeletal muscle; FABPpm in adipose tissue) were attributable to their increased expression, whereas in liver, the reduced plasma membrane FABPpm appeared to be due to its relocation within the cell in the face of slightly increased expression. Taken together, STZ-induced changes in fatty acid uptake demonstrate a complex and tissue-specific pattern, involving different fatty acid transporters in different tissues, in combination with different underlying mechanisms to alter their surface abundance.

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“…While MCT1 is generally localised to the plasma membrane (Philp et al 1998, 2003a, 2003b, Bergersen et al 1999, Fanelli et al 2003, Clamp et al 2004, tissue fractionation has revealed MCT1 in sarcoplasmic reticulum, T-tubules, triads, and intracellular membranes of rat heart and skeletal muscle (Bonen et al 2000) and in rat liver peroxisomes (McClelland et al 2003). These data are consistent with our finding that MCT1 immunoreactivity, while it appears brighter in the cytoplasmic cortex of cleavage-stage embryos, persists diffusely in the cytoplasm of morulae and early blastocysts.…”

Section: Effect Of Glucose On Mct Expression In Vitromentioning

confidence: 99%

Glucose affects monocarboxylate cotransporter (MCT) 1 expression during mouse preimplantation development

Jansen¹,

Esmaeilpour²,

Pantaleon³

et al. 2006

Reproduction

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Cleavage-stage embryos have an absolute requirement for pyruvate and lactate, but as the morula compacts, it switches to glucose as the preferred energy source to fuel glycolysis. Substrates such as glucose, amino acids, and lactate are moved into and out of cells by facilitated diffusion. In the case of lactate and pyruvate, this occurs via H 1 -monocarboxylate cotransporter (MCT) proteins. To clarify the role of MCT in development, transport characteristics for DL-lactate were examined, as were mRNA expression and protein localisation for MCT1 and MCT3, using confocal laser scanning immunofluorescence in freshly collected and cultured embryos. Blastocysts demonstrated significantly higher affinity for DL-lactate than zygotes (K m 20 6 10 vs 87 6 35 mmol lactate/l; P 5 0.03 by linear regression) but was similar for all stages. For embryos derived in vivo and those cultured with glucose, MCT1 mRNA was present throughout preimplantation development, protein immunoreactivity appearing diffuse throughout the cytoplasm with brightest intensity in the outer cortical region of blastomeres. In expanding blastocysts, MCT1 became more prominent in the cytoplasmic cortex of blastomeres, with brightest intensity in the polar trophectoderm. Without glucose, MCT1 mRNA was not expressed, and immunoreactivity dramatically reduced in intensity as morulae died. MCT3 mRNA and immunoreactivity were not detected in early embryos. The differential expression of MCT1 in the presence or absence of glucose demonstrates that it is important in the critical regulation of pH and monocarboxylate transport during preimplantation development, and implies a role for glucose in the control of MCT1, but not MCT3, expression.

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Abundance and subcellular distribution of MCT1 and MCT4 in heart and fast-twitch skeletal muscles

Cited by 94 publications

References 35 publications

Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane

Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane

Changes in fatty acid transport and transporters are related to the severity of insulin deficiency

Glucose affects monocarboxylate cotransporter (MCT) 1 expression during mouse preimplantation development

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