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Fumonisin toxicity mainly disrupts sphingolipid metabolism by inhibiting ceramide synthase, the enzyme that converts sphinganine to ceramide. This blocks a central step in sphingolipid biosynthesis, leading to buildup of sphinganine (and related sphingoid bases) and a shortage of downstream sphingolipids needed for normal cell membranes and signaling.

Because sphingolipids are fundamental to membrane integrity and cell signaling, this disruption causes cellular injury across organs, with the liver commonly showing dysfunction due to its central role in lipid metabolism and detoxification. A practical biomarker is an increased sphinganine level relative to sphingosine in tissues or blood, reflecting interference with ceramide synthesis.

Note that other species-specific effects can occur (e.g., neurologic disease in horses, pulmonary edema in pigs), but the shared mechanism is inhibition of sphingolipid biosynthesis, leading to hepatic dysfunction as a characteristic consequence.