Carrying fatty acids across a barrier they cannot cross alone
Long-chain fatty acids cannot pass through the inner mitochondrial membrane on their own, which is where carnitine becomes essential. An enzyme called CPT1 attaches the fatty acid to carnitine on the outer side, a transporter moves the resulting acylcarnitine across the membrane, and CPT2 releases the fatty acid inside so beta-oxidation can proceed. This carnitine shuttle is the gateway controlling how quickly long-chain fat can be delivered for burning, and it is one of the main regulated steps in fat metabolism.
Because the shuttle is a control point, it is often assumed that adding carnitine will speed fat burning, but availability is not usually the limiting factor in healthy, well-nourished people.
Why supplementing rarely moves the needle
Healthy people generally maintain adequate muscle carnitine, and oral carnitine is poorly taken up by muscle, so supplementation does not reliably raise muscle stores or accelerate fat loss in most studies. Carnitine has clearer relevance in specific clinical deficiency states, which are different from the general fat-loss context in which it is marketed.
This is general educational information about a mechanism, not medical or supplementation advice. Carnitine should not be assumed to cause fat loss, and anyone with a medical condition should consult a qualified professional before use.