Cold-induced metabolism
article
Purpose of review
Cold response can be insulative (drop in peripheral temperature) or metabolic (increase in energy expenditure). Nonshivering thermogenesis by sympathetic, norepinephrine-induced mitochondrial heat production in brown adipose tissue is a well known component of this metabolic response in infants and several animal species. In adult humans, however, its role is less clear. Here we explore recent findings on the role and variability of nonshivering thermogenesis in adults.
Recent findings
Large individual differences exist in mild cold response with respect to the relative contribution of the insulative response and the metabolic (nonshivering) response. In search for the possible explanations of this variation, recent studies on potential mechanisms of nonshivering thermogenesis in humans are presented. Emphasis is given to the role of uncoupling proteins, mitochondrial ATP-synthase, and calcium cycling. The potential contribution of human skeletal muscle to nonshivering thermogenesis is discussed. The differences in nonshivering thermogenesis can partly be attributed to factors such as age, gender, physical fitness, adaptation, and diet. There are indications that genetic variation affect cold response.
Summary
The implications of the observed large individual variation in cold response is that a low metabolic response to cold can partly explain increased risk to develop obesity. Both the effect of environmental factors and genetic factors on nonshivering thermogenesis require more well controlled studies. With extended knowledge on these factors it can be ascertained if a pharmacological regimen is possible which would mimic the effects of chronic cold or elevated catecholamine levels, without attendant side effects.
Cold response can be insulative (drop in peripheral temperature) or metabolic (increase in energy expenditure). Nonshivering thermogenesis by sympathetic, norepinephrine-induced mitochondrial heat production in brown adipose tissue is a well known component of this metabolic response in infants and several animal species. In adult humans, however, its role is less clear. Here we explore recent findings on the role and variability of nonshivering thermogenesis in adults.
Recent findings
Large individual differences exist in mild cold response with respect to the relative contribution of the insulative response and the metabolic (nonshivering) response. In search for the possible explanations of this variation, recent studies on potential mechanisms of nonshivering thermogenesis in humans are presented. Emphasis is given to the role of uncoupling proteins, mitochondrial ATP-synthase, and calcium cycling. The potential contribution of human skeletal muscle to nonshivering thermogenesis is discussed. The differences in nonshivering thermogenesis can partly be attributed to factors such as age, gender, physical fitness, adaptation, and diet. There are indications that genetic variation affect cold response.
Summary
The implications of the observed large individual variation in cold response is that a low metabolic response to cold can partly explain increased risk to develop obesity. Both the effect of environmental factors and genetic factors on nonshivering thermogenesis require more well controlled studies. With extended knowledge on these factors it can be ascertained if a pharmacological regimen is possible which would mimic the effects of chronic cold or elevated catecholamine levels, without attendant side effects.
Topics
AdaptationCold toleranceEnergy expenditureEffects of coldAdaptive thermogenesisBrown adipose tissueCold responseEnergy expenditureNonshivering thermogenesisUncoupling proteinsBody compositionCalcium signalingCold exposureDietary intakeEnergy expenditureEnergy metabolismEnvironmental factorFitnessGeneticsNonshivering thermogenesisSkeletal muscleStimulus responsethermogenesisAdipose Tissue, BrownBody Temperature RegulationColdHumansShiveringThermogenesisAnimalia
TNO Identifier
11957
Source
Current Opinion in Clinical Nutrition and Metabolic Care, 6(4), pp. 469 - 475.
Pages
469 - 475