Potential contribution of vasoconstriction to suppression of heat loss and homeothermic regulation in UCP1-deficient mice

To investigate the thermoregulatory mechanism in mice lacking uncoupling protein 1 (UCP1) from the viewpoint of heat loss, we measured oxygen consumptions (VO2), skin-surface temperatures (Tskin, an index of heat release), blood flows in the tails, and rectal temperatures (Trectal) of mice housed in an animal room under the standard thermal condition of ∼23°C. Compared with wildtype (Ucp1^+/+) mice, adult UCP1-deficient (Ucp1 ^-/-) mice tended to show a reduced VO2. Thermograhic analysis of the acute response of Ucp1^-/- mice to a small change (a drop of 1-2°C) in the ambient temperature revealed a sustained fall in the Tskin of Ucp1^-/- mice; but this fall was only transient in Ucp1^+/+ mice. Analysis of tail blood flow under anesthesia clearly showed a stronger vasoconstrictor response in Ucp1^-/- mice than in Ucp1^+/+ mice. Administration of a vasodilator, evodiamine, transiently increased Tskin in Ucp1^+/+ and Ucp1^-/- mice similarly; whereas the induction of vasodilation caused a greater and more prolonged reduction in Trectal in Ucp1^-/- mice than in Ucp1^+l+ mice. These results indicate that Ucp1^-/- mice highly, or at least partly, rely on vasoconstriction for heat conservation to compensate for their UCP1 deficiency and to maintain homeothermy under the condition of normal housing temperature.