to the editor: Fischer et al. (2) reported that obesity does not serve as an insulator in mice and on this basis questioned whether the prevailing wisdom that obese humans are better insulated than their lean counterparts is actually correct. The motivation for their study was that insulation from fat might aggravate obesity, as the thermogenic requirement for thermoregulation in the cold would be diminished. Nevertheless, the authors assert that their findings “may not have a discernible effect on the development of human obesity” because they reside primarily under conditions eliciting minimal thermogenic requirements. Profound metabolic benefits of activating brown adipose tissue (BAT) in humans at the cooler end of the thermoneutral scale have been proposed (4), and extra insulation from dermal fat in obese individuals would likely compromise BAT activation. So whether obesity in humans provides an insulating effect is indeed an important question. However, two issues substantially limit the transferability of the present findings (2) to humans.
Higher levels of adipose tissue in humans have repeatedly been shown to provide an insulating effect. During cold water immersion, stable body temperatures at lower water temperatures are evident with greater fat mass (3). Importantly, this insulating effect of fat, particularly during milder cold exposures, is dependent upon a strong, cold-induced cutaneous vasoconstriction (5), as a substantial proportion of fat in most humans is subcutaneous. Although the majority of adipose tissue in mice is not subcutaneous, the authors reported thicker dermal fat layers in obese mice (2). However, since mice chiefly demonstrate a strong vasoconstriction in the tail, ear, and feet, where excess body fat is not located, the absence of an insulating effect with this model should not be surprising.
The authors provided a solid, metabolically related rationale for expressing energy expenditure in units per kilogram lean body mass (2). But human heat balance theory (5) states that for core temperature to be successfully defended, the absolute rate of net heat dissipation from the body surface to the surrounding environment, which is determined by surface area, must be balanced by the absolute rate that heat is internally generated by metabolism. Obese mice are larger than lean mice, and therefore, they have a greater surface area. For example, at a 4°C acclimation temperature, high-fat diet (HFD) mice were 48.8 g, whereas chow mice were 31.5 g, which according to Dawson (1) would have given surface areas of 102 and 85 cm2, respectively. If obesity did not provide any additional insulation, the absolute rate of heat loss and, therefore, the absolute energy expenditure needed to attain heat balance would have been proportionally greater in the larger, obese mice. But dividing these different absolute metabolic requirements for heat balance by the similar lean mass between obese (HFD: 22.6 g) and lean (chow: 21.8 g) mice should have resulted in a greater required energy expenditure per kilogram lean mass and greater Scholander plot slopes with declining ambient temperature in obese mice. Therefore, the similar energy expenditures actually indicate some potential insulating effects of obesity in mice after all.
No conflicts of interest, financial or otherwise, are declared by the authors.
O.J. drafted manuscript; O.J. and D.R. edited and revised manuscript; O.J. and D.R. approved final version of manuscript.
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