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The chain-length-resolved acylcarnitine data revealed a pattern that contradicted the prevailing model: Why It Matters The chain-length pattern told a story that no single measurement could: short-chain species (C2, C4) were elevated because beta-oxidation was running at oull speed but the TCA cycle couldn't oxidize all the acetyl-CoA produced, causing incomplete oxidation and acylcarnitine "spillover." Meanwhile, long-chain species (C14, C16) were elevated because excess dietary lipid supply simply overloaded CPT-I import capacity

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Without that contrast, this exact same technique would read flat