Abstract
SYNOPSIS. Evidence in support of the hypothesis that T3-induced enhancement of O2 consumption in mammalian target tissues is attributable to a stimulation of energy utilization for active transmembrane Na$ and K$ transport is reviewed. The stimulation of target-tissue Na, K transport-dependent respiration following T3 treatment is associated with enhanced rates of active Na$ efflux and K$ influx as well as with an increase in Na, KATPaseenzymatic activity. The enhancement of Na, K-ATPase activity and enzyme abundance is secondary to a T3-induced stimulation of Na, K-ATPase a and rβ subunit biosynthesis and is probably mediated by increased abundance of specific messenger RNAs coding for the subunits of the enzyme. It is proposed that a coordinate augmentation of Na, KATPase enzymatic activity and enhancement of passive membrane permeability to Na$ and K$ are necessary to maintain the increased rates of active Na, K transport and energy consumption associated with thyroid thermogenesis.

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