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Figure 3. Model illustrating the mechanisms by which an up-regulation of SCD1 in skeletal muscle might lead to suppressed thermogenesis. In fed state (A), repeated recycling of acetyl-coenzyme A through flux of substrates across de novo lipogenesis followed by mitochondrial ß-oxidation constitutes an energy dissipating "substrate cycling" in skeletal muscle. During semistarvation and early refeeding (B), an elevated SCD1 would, by enhancing the desaturation of de novo synthesized fatty acids, divert them away from pathways of mitochondrial ß-oxidation and effectively shut down this thermogenic substrate cycling mechanism, thereby leading to energy conservation.
