Wang · The American journal of physiology 1996 · in vitro mechanistic cellular assay · n=?

Substrate and inhibitor specificities of the monocarboxylate transporters of single rat heart cells.

Cited 61 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

In vitro laboratory study using isolated animal cells.

PubMed 8779821 · doi:10.1152/ajpheart.1996.270.2.H476 · record verified 2026-08-30

What was done

The authors characterized the substrate and inhibitor kinetics of monocarboxylate transport in isolated single rat heart cells using the intracellular pH-sensitive fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). They measured transport rates and inhibition profiles across multiple substituted monocarboxylates (C2–C5) and specific chemical inhibitors.

What was found

The study identified two distinct lactate transport carriers in rat heart cells, both differing from MCT-1: - One carrier was inhibited by alpha-cyano-4-hydroxycinnamate (CHC; Ki = 190 µM) and stilbene disulfonates (Ki = 79 µM for 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid; Ki = 38 µM and 171 µM for cis- and trans-isomers of 4,4'-dinitrostilbene-2,2'-disulfonate, respectively). - The second carrier showed markedly lower sensitivity to CHC (Ki ≈ 3 mM) and stilbene disulfonates (Ki = 0.5–2 mM). - Both carriers were inhibited by 3-isobutyl-1-methylxanthine (Ki = 340 µM), and neither was inhibited by 5-nitro-2-(3-phenylpropylamino)benzoate. - Overall Km values for the ketone bodies D-beta-hydroxybutyrate and acetoacetate were 10 mM and 5.4 mM, respectively, with Vmax values similar to L-lactate and pyruvate. - No stereoselectivity was observed between L- and D-isomers of 2-chloro or 2-hydroxy acids.

Why it matters

The findings show that rat cardiac cells possess transporter isoforms distinct from MCT-1 requiring unusually high inhibitor concentrations for complete blockade, and indicate that ketone body transport capacity may restrict the rate of myocardial ketone metabolism under physiological conditions.

Limits

This was an in vitro study conducted exclusively on isolated rat cardiomyocytes, which may not fully mirror in vivo intact organ physiology or human myocardium. The experimental approach measured overall transport kinetics and could not separate the individual kinetic parameters (Km and Vmax) of each specific transporter isoform. Sample size (number of animals or cells analyzed) was not reported in the abstract.

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