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So with this basic understanding that OCTN2 is a cotransporter of sodium & carnitine and that under normal conditions it is fully saturated and thus unable to benefit further carnitine inflow via Na+/K+ ATPase pump activity, lets examine how insulin overcomes this equilibrium and brings about an increased inflow of carnitine into skeletal muscle

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Black SM, Wolf CR (1991) The role of glutathione-dependent enzymes in drug resistance

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