In mammals the desaturation of saturated and polyunsaturated fatty acids (PUFA) is almost exclusively considered separately: the FADS genes apply to PUFA and the SCD apply to saturates
Palmitic acid is the only exception, being a substrate for both SCD (16:0➔16:1n-7) and FADS2 (16:0➔16:1n-10)
Competition experiments shows excess of 16:0 suppresses endogenous eicosanoid and docosanoid precursor synthesis by competing for FADS2 mediated desaturation with essential PUFA
Metabolic conditions that induce local excess of 16:0 such as excess carbohydrate intake can inhibit synthesis of PUFA precursors for membrane synthesis and alter signaling precursors