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The "nicotinic acid pathway" is a set of metabolic routes responsible for the biosynthesis of nicotinamide adenine dinucleotide (NAD⁺) from dietary precursors such as nicotinic acid (niacin), nicotinamide, nicotinamide riboside, and tryptophan. The principal routes include the Preiss-Handler pathway (nicotinic acid → NAD⁺), the de novo pathway from tryptophan, and the salvage pathway from nicotinamide. These pathways are crucial for cellular energy production, redox reactions, and multiple signaling processes. Pharmacologically, niacin impacts lipid metabolism via G-protein coupled receptors (HCA₂, HCA₃), making it therapeutically relevant for dyslipidemia, but the pathway itself is not a single protein or receptor. NAD⁺ biosynthesis defects cause diseases such as pellagra and potentially contribute to aging and metabolic conditions.
NAD⁺ precursor supplementation increases cellular NAD⁺; Niacin activates hydroxycarboxylic acid receptors (HCA₂/GPR109A and HCA₃/GPR109B), leading to lipid-modifying effects.
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