Elevated fatty acid (FA) levels contribute to severe metabolic diseases. Unbalanced
oversupply of saturated FAs is particularly damaging, which renders stearoyl-CoA desaturase
(SCD1) activity an important factor of resistance. A SCD1-related oxidoreductase protects
cells against palmitate toxicity, so we aimed to test whether desaturase activity
is limited by SCD1 itself or by the associated electron supply. Unsaturated/saturated
FA ratio was markedly elevated by SCD1 overexpression while it remained unaffected
by the overexpression of SCD1-related electron transfer proteins in HEK293T cells.
Electron supply was not rate-limiting either in palmitate-treated cells or in cells
with enhanced SCD1 expression. Our findings indicate the rate-limiting role of SCD1
itself, and that FA desaturation cannot be facilitated by reinforcing the electron
supply of the enzyme.
