Lipid metabolism during cold-exposure and during cold-acclimation
- Cite this article as:
- Himms-Hagen, J. Lipids (1972) 7: 310. doi:10.1007/BF02532649
- 133 Downloads
The lipid-containing tissues are important in cold-exposure (exposure to cold of animals not previously living in the cold) and in cold-acclimation (the adaptive state achieved when animals have lived in the cold for several weeks); these are the white adipose tissue and the brown adipose tissue. The white adipose tissue serves as a store of readily mobilized substrate (free fatty acids [FFA]) for calorigenesis in other tissues during cold-exposure, principally for shivering thermogenesis in muscle. The mobilization of the sterol lipid is brought about through activation of the sympathetic nervous system by the cold stress. The brown adipose tissue has two functions in cold-exposure and in cold-adaptation, both quite distinct from the function of the white adipose tissue. These functions are heat production and the maintenance of the adaptationto cold. The triglycerides stored in the brown adipose tissue are mobilized as FFA, also via activation of the sympathetic nervous system, but the FFA are used primarily within the brown adipose tissue itself. The FFA are the agents which switch on the calorigenesis in the brown adipose tissue (via a poorly understood form of “loosening” of the coupling of oxidative phosphorylation); they also serve as the substrate for the calorigenesis. The heat-producing function of the brown adipose tissue occurs in both cold-exposed and in cold-acclimated animals; it is of greater importance in the latter because this tissue normally grows in response to cold. Much of the heat production in cold-acclimated animals (nonshivering thermogenesis) occurs outside the brown adipose tissue itself, most probably in the muscles, and the cold-acclimated animal differs from the cold-exposed animal in being able to switch on nonshivering thermogenesis via activation of the sympathetic nervous system. The maintenance of this adaptation for nonshivering thermogenesis in tissue other than the brown adipose tissue itself depends upon the brown adipose tissue. The adaptation disappears if the brown adipose tissue is removed; the adaptation does not develop if the normal proliferation of mitochondria in the growing brown adipose tissue is inhibited (with oxytetracycline) during acclimation of rats to cold. The mechanism by which the brown adipose tissue exerts this second function is at present unknown. An increased turnover of certain mitochondrial proteins occurs in those tissues (skeletal muscle and brown adipose tissue) in which nonshivering thermogenesis occurs in cold-acclimated rats; no change in turnover of mitochondrial proteins occurs in other tissues (liver and kidney). The relation of this alteration in mitochondrial proteins to the adaptation for nonshivering thermogenesis is at present unknown. However this first demonstration of a biochemical difference between skeletal muscle of cold-acclimated rats and skeletal muscle of warm-acclimated rats opens up a new approach to the study of the nature of both the adaptation for nonshivering thermogenesis and of the role of the brown adipose tissue in the development and maintenance of this adaptation.