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 approximately 23 degrees C. Compared with wild-type (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 degrees 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+/+ 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.