Monocarboxylic acid transporter 1 (MCT1) expression in developing rat brain

B. E. Enerson, O. Zhdankina, D. Z. Gerhart, Lester R Drewes

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Monocarboxylates, such as lactate, pyruvate, 2-hydroxybutyrate, and acetoacetate are important metabolic fuels in the developing rat brain. We have previously reported that a monocarboxylic acid transporter (MCT1) is significantly expressed in rat brain (Gerhart et al, Am. J. Physiol. 273: E207-E213, 1997). Because brain endothelial cells in suckling rat express MCT1 protein at levels substantially greater than adults, MCT1 may play a key role in delivery of monocarboxylates to the developing brain. The purpose of this study was to elucidate the developmental expression of this transporter. Western blots of whole-brain membrane fractions derived from rats of various ages were performed using an antibody against rat MCT1. The results indicate a linear increase in the relative amount of MCT1 from P2 to P21. At P21 (n=5) the relative amount of MCT1 is approximately 5-fold that of P2 (n=3). The relative amount of protein in rats older than P21 was unchanged. To characterize further this developmental change, ribonuclease protection assays were performed on total RNA isolated from whole brains of rats at various stages of development. The relative amount of MCT1 mRNA in rats P0 to P21 increased in a manner similar to that found for the MCT1 protein. However, in rats older than P21 there was a significant drop in mRNA. Taken together, this data indicates a significant increase in the expression of MCT1 in rat brain during development until approximately 21 days. After 21 days the amount of MCT1 mRNA decreases while the relative amount of protein does not. Thus, it is suggested that a change in the transcriptional or translational regulation of brain MTC1 occurs during development.

Original languageEnglish (US)
Pages (from-to)A1032
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998

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