Biological Significance

Such an adaptive phenomenon that accelerates the restitution of fat stores rather than diverting the energy saved toward compensatory increases in body protein synthesis (an energetically costly process) would have survival value in ancestral famine-and-feast lifestyle. This is because by virtue of the fact that body fat has a greater energy density and a lower energy cost of synthesis/maintenance than protein, it would provide the organism with a greater capacity to rapidly rebuild an efficient energy reserve and hence to cope with recurrent food shortage. Thus, the functional role of the adipose-specific control of thermogenesis during weight recovery is to accelerate specifically the replenishment of the fat stores whenever food availability is increased after a long period of food deficit and severe depletion of body fat stores. It provides an alternative mechanism to recover survival capacity in the absence of hyperphagia. However, equally important for the survival of mammals during weight loss and weight recovery is the need to retain the capacity to increase heat production (i.e., to activate thermogenesis) in response to a number of other environmental stresses, namely (i) for increased thermoregulatory needs in cold environments, (ii) for the generation of fever during exposure to infections, or (iii) for increased heat production as an adaptation to nutrient-deficient diets. The necessity to increase DIT in the face of nutrient-deficient diets probably had evolutionary survival advantage of 'homeostatic waste' because it enables individuals to overeat relatively large quantities of poor-quality food in order to obtain essential nutrients without the deposition of excess, nonessential energy as fat. Excessive weight gain would be a hindrance to optimal locomotion, hunting capabilities, and the ability to fight or flee. It has been proposed that DIT may have evolved as a means of regulating the metabolic supply of essential nutrients (protein, minerals, and vitamins) with only a secondary role in regulating energy balance and body weight. Whatever the exact functional significance of DIT, however, it is clear that in the context of weight recovery an elevated efficiency for catchup fat can be shown to persist even under conditions of hypermetabolism (a net increase in thermogen-esis) induced by hyperphagia or nutrient-deficient diets. To explain this apparent paradox, the model presented in Figure 4 provides a structural framework that illustrates how suppressed adipose-specific thermogenesis that results in enhanced fat deposition during refeeding, and that is postulated to occur in the skeletal muscle, persists under conditions when the nonspecific control of thermogen-esis is activated in organs/tissues recruited by the SNS (liver, kidneys, heart, and brown adipose tissue). Such differentially regulated control systems for thermogenesis may thus have arisen during the course of mammalian evolution as dual-adaptive processes that can satisfy the need for energy conservation during weight loss or for catch-up fat during weight recovery, even under environmental stresses when SNS-mediated activation of heat production has equally important survival values.

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