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“Lipoic acid absorption” is not a discrete molecule, receptor, transporter, or enzyme; it describes the pharmacokinetic process by which alpha-lipoic acid (thioctic acid) from supplements or diet is absorbed in the gastrointestinal tract. Human and in vitro data indicate that oral alpha-lipoic acid is variably absorbed (about 30–40% for typical racemic oral doses), with faster and greater absorption in the fasting state than with food; peak plasma concentrations typically occur within 0.5–1 hour fasting, and food can reduce Cmax by ~30% and overall exposure by ~20%[1][5][6][7]. Mechanistically, studies support transporter-mediated uptake: evidence implicates the sodium-dependent multivitamin transporter (SMVT; SLC5A6) as a Na+-dependent carrier for lipoic acid, and inhibition studies in Caco-2 cells suggest participation of proton-linked monocarboxylate transport at acidic pH; uptake is energy-dependent and pH-sensitive[2][4][3]. Therefore, while “lipoic acid absorption” is not itself a therapeutic target, specific transporters involved in lipoic acid uptake—such as SMVT and potentially monocarboxylate transporters—are bona fide molecular entities.
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