Barbara Cannon's data on the UCP1-ablated mice: "Non-cannonical" point of view

The data of Cannon and co-workers on UCP1-ablated mice are interpreted assu ming that UCP2 and UCP3 are involved in thermoregulation as fatty acid-depe ndent uncouplers although they are not sufficient, in the absence of UCP1, for long term maintenance of normal body temperature of mice after sudden a nd strong decrease in the ambient temperature. I would like to suggest that in brown fat of control mice, UCP1 is present in an amount higher than UCP 2 and 3 and, therefore, is able to cause (a) some fatty acid-mediated decre ase in proton motive force in resting state and, hence, (b) oxidation of Co QH(2) to CoQ which is shown by Klingenberg and coworkers to be cofactor for UCPs. This results in strong uncoupling and thermogenesis mediated by UCP1 , 2 and 3. In the UCP1-ablated mice, activity of UCP2 and 3 appears to be i nsufficient to induce CoQH(2) oxidation in resting brown fat mitochondria, which results in hypothermia.