Contribution of the mouse tail to heat dissipation
Authors: Skop Vojtech , Liu Naili , Gavrilova Oksana , Reitman Marc 
Published: April 2020

Mice are widely used to study obesity and diabetes. Since there are big differences in thermal physiology between mice and humans, understanding these differences is important for using mice predictively to model human disease. Heat dissipation is limited in mice, as they do not routinely use evaporative heat loss. The mouse tail contributes to non‐evaporative heat loss, as it has no hair, a large surface to volume ratio, and dense vascularization. The rat tail has been reported to dissipate ~20 % of body heat, but we are unaware of a similar analysis for mice. Scaling and other considerations suggest that the mouse tail is relatively less effective for heat dissipation. Here, we used tailless mice to quantitate the capacity of the mouse tail to dissipate heat.

C57BL/6J mice had their tails amputated shortly after birth and were compared to littermate controls. Total energy expenditure (TEE) was determined by indirect calorimetry or estimated from energy balance. Core body temperature (Tb) was measured using intraperitoneal radiotelemetry probes, surface temperature was measured by infrared thermography, and body composition was measured by magnetic resonance spectroscopy (EchoMRI).

Tailless mice did not differ from controls in body weight, lean or fat content, or TEE (22 °C). Tb of tailless and control mice was not different at ambient temperatures (Ta) of 22 °C, 31 °C, or 34°C. We reasoned that a Scholander‐type of analysis (of TEE vs Ta, over a wide Ta range) might detect subtle differences in thermal physiology. However, no differences were observed in Tb or TEE between tailless and control mice. To maximize the need for heat dissipation, brown adipose tissue thermogenesis was activated by treatment at 30 °C with CL316243, a β3‐adrenergic receptor agonist. This treatment increased TEE from 0.263 ± 0.011 kcal/h to 0.490 ± 0.033 kcal/h and Tb from 36.0± 0.2 °C 37.5 ± 0.3 °C in controls. Both parameters increased more in tailless mice; TEE from 0.264 ±0.016 kcal/h to 0.557 ± 0.032 kcal/h and Tb from 36.1 ± 0.2 °C to 38.3 ± 0.2 °C, indicating that the tail does contribute to heat dissipation under heat stress conditions. The tail is normally vasoconstricted at 22 °C. To enhance tail heat dissipation, peripheral vasodilation was achieved using prazosin, an α1‐adrenergic receptor antagonist, which increased tail temperature from 23.7 ± 0.9 °C to 29.1 ± 1.9 °C and increased heat loss by 10 % in control mice. In tailless mice, the increase in total heat loss after prazosin treatment was reduced to 5 %. Thus, in this experiment, the tail contributed 5 % of total heat dissipation (0.02 kcal/h), equal to 9 % of the BMR.

These results demonstrate that the mouse tail contribution to heat dissipation is detectable under conditions of heat stress, however the contribution is modest. Experimentally, the tail is an accessible indicator of the heat status of the mouse. Understanding the tail’s role in mouse thermal biology enriches and informs the use of the mouse as a model organism for studying energy homeostasis, diabetes, and obesity.

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