Triiodothyroacetic acid (Triac) is a physiological product of T3 metabolism, with high affinity for T3 nuclear receptors. Its interest stems from its potential thermogenic effects. Thus, this work aimed: 1) to clarify these thermogenic effects mediated by Triac versus T3 in vivo and 2) to determine whether they occurred predominantly in adipose tissues. To examine this, control rats were infused with equimolar T3 or Triac doses (0.8 or 4 nmols /100g BW/day) or exposed 48 h to cold. Both T3 doses and only the highest Triac dose inhibited plasma and pituitary TSH and T4 in plasma and tissues. Interestingly, the lower Triac dose marginally inhibited plasma T4. T3 infusion increased plasma and tissues T3 in a tissue-specific manner. The highest Triac dose increased Triac concentrations in plasma and tissues, decreasing plasma T3. Triac concentrations in tissues were <10% those of T3. Under cold exposure or high T3 doses, Triac increased only in white adipose tissue (WAT). Remarkably, only the lower Triac dose activated thermogenesis, inducing ectopic UCP-1 expression in WAT and maximal increases in UCP-1, UCP-2 and LPL expression in brown adipose tissue (BAT), inhibiting UCP-2 in muscle and LPL in WAT. Triac, T3 and cold exposure inhibited leptin secretion and mRNA in WAT. In summary, Triac, at low doses, induces thermogenic effects in adipose tissues without concomitant inhibition of TSH or hypothyroxinemia, suggesting a specific role regulating energy balance. This selective effect of Triac in adipose tissues might be considered as a potential tool to increase energy metabolism.