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Mitochondrial acetyl-CoA primarily derives from pyruvate dehydrogenase-mediated oxidative decarboxylation, with additional sources including fatty acid β-oxidation, catabolism of branched-chain amino acids (leucine/isoleucine), ketone body breakdown (e.g., β-hydroxybutyrate), and ATP-dependent acetate activation ( Figure 1 FASN catalyzes the elongation cycle by sequentially adding malonyl-CoA units to acetyl-CoA (with NADPH as the reductant) to generate palmitate (a 16-carbon saturated fatty acid) ( + intestinal stem cell function ( Following palmitate synthesis, elongation by ELOVL enzymes produces stearate and longer-chain saturated fatty acids (SFAs) (98, 99), and chemoresistance (100), whereas intestinal SCD1 knockout in mice exacerbates inflammation and tumorigenesis—phenotypes reversible by oleate supplementation (101)
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