Non‐shivering Thermogenesis and Its Thermoregulatory Significance

Janský, L

doi:10.1111/j.1469-185x.1973.tb01115.x

Cited by 561 publications

(91 citation statements)

References 160 publications

(71 reference statements)

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“…An underestimated phenomenon is that thermogenesis is primarily achieved through muscular shivering in the hours to days of exposure to cold but is progressively replaced by adaptive nonshivering thermogenesis (Fig. 1A) (Janský, 1973;Klingenspor, 2003;Cannon and Nedergaard, 2004;Ouellet et al, 2012). This latter process is achieved through mitochondrial uncoupling via UCP1 in the brown adipose tissue (extensively reviewed by Cannon and Nedergaard, 2004).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial uncoupling prevents cold-induced oxidative stress: a case study using UCP1 knock-out mice

Stier

Bize

Habold

et al. 2013

Journal of Experimental Biology

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The relationship between metabolism and reactive oxygen species (ROS) production by the mitochondria has often been (wrongly) viewed as straightforward, with increased metabolism leading to higher generation of pro-oxidants. Insights into mitochondrial functioning show that oxygen consumption is principally coupled with either energy conversion as ATP or as heat, depending on whether the ATP-synthase or the mitochondrial uncoupling protein 1 (UCP1) is driving respiration. However, these two processes might greatly differ in terms of oxidative costs. We used a cold challenge to investigate the oxidative stress consequences of an increased metabolism achieved either by the activation of an uncoupled mechanism (i.e. UCP1 activity) in the brown adipose tissue (BAT) of wild-type mice or by ATP-dependent muscular shivering thermogenesis in mice deficient for UCP1. Although both mouse strains increased their metabolism by more than twofold when acclimatised for 4 weeks to moderate cold (12°C), only mice deficient for UCP1 suffered from elevated levels of oxidative stress. When exposed to cold, mice deficient for UCP1 showed an increase of 20.2% in plasmatic reactive oxygen metabolites, 81.8% in muscular oxidized glutathione and 47.1% in muscular protein carbonyls. In contrast, there was no evidence of elevated levels of oxidative stress in the plasma, muscles or BAT of wild-type mice exposed to cold despite a drastic increase in BAT activity. Our study demonstrates differing oxidative costs linked to the functioning of two highly metabolically active organs during thermogenesis, and advises careful consideration of mitochondrial functioning when investigating the links between metabolism and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial uncoupling prevents cold-induced oxidative stress: a case study using UCP1 knock-out mice

Stier

Bize

Habold

et al. 2013

Journal of Experimental Biology

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“…The most effective way of reducing heat loss in the animal is through skin vasoconstriction (13). Increased heat production or thermogenesis can be achieved via two mechanisms: shivering thermogenesis if the heat comes from contracting skeletal muscles (15) or nonshivering thermogenesis if it comes from elsewhere (13,17). The best studied effector of nonshivering thermogenesis is brown adipose tissue (BAT), which is under sympathetic control (4,20).…”

mentioning

confidence: 99%

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

Marks¹,

Vianna²,

Carrive³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Marks A, Vianna DM, Carrive P. Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat. Am J Physiol Regul Integr Comp Physiol 296: R1239 -R1247, 2009. First published February 11, 2009 doi:10.1152/ajpregu.90723.2008.-As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via ␤-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the ␤-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a ϩ1.5°C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap Ϫ TBack) by ϩ1°C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4°C) induced a ϩ2.7°C increase in TiScap-TBack, which was reduced to ϩ1°C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by ␤-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either. stress hyperthermia; thermoregulation; tail skin; freezing; sympathetic responses MANY PSYCHOLOGICAL STRESSORS can cause an increase in body temperature (2,11,25,29), an effect also known as stress hyperthermia (2, 18). There are two ways in which body temperature can be elevated, either by reducing heat loss or by increasing heat production. The most effective way of reducing heat loss in the animal is through skin vasoconstriction (13). Increased heat production or thermogenesis can be achieved via two mechanisms: shivering thermogenesis if the heat comes from contracting skeletal muscles (15) or nonshivering thermogenesis if it comes from elsewhere (13, 17). The best studied effector of nonshivering thermogenesis is brown adipose tissue (BAT), which is under sympathetic control (4, 20). Only present in mammals, BAT is classically called into action during cold exposure. It is most often found in newborns, small mammals, and hibernating species, which are the ones who are most prone to suffer from cold stress, but it might also be functional in adult humans (6,20). Moreover, it is the only site where cold adaptation, that is, the development of increased recruitable thermogenic capacity in response to chronic cold exposure, occurs (4, 9, 12). In rats and ...

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“…The two stable consecutive highest values were taken to calculate maximum NST (Li and Wang, 2005;Wang and Wang, 1996). NST capacity (NST cap ) was calculated as the maximum NST minus RMR at thermal neutral zone (Jansky, 1973;Klaus et al, 1988). …”

Section: Metabolic Trialsmentioning

confidence: 99%

“…In some species such as Siberian hamsters (Phodopus sungorus), SD acclimation increased non-shivering thermogenesis (NST) and UCP1 content . NST is an important mechanism for thermoregulation in small mammals (Jansky, 1973) and BAT is a major site for NST (Ricquier and Bouillaud, 2000). The enhancement of BAT function is fulfilled by increasing BAT mass, mitochondrial protein (MP) content (Martin et al, 1989;Trayhurn et al, 1982) and, most importantly, increased expression of UCP1.…”

Section: Introductionmentioning

confidence: 99%

Effects of photoperiod history on body mass and energy metabolism in Brandt's voles (Lasiopodomys brandtii)

Zhong

Wang

2007

Journal of Experimental Biology

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SUMMARY Many small mammals respond to seasonal changes in photoperiod via alterations in morphology, physiology and behaviour. In the present study, we tested the hypothesis that the preweaning (from embryo to weaning) photoperiod experience can affect subsequent development in terms of body mass and thermogenesis. Brandt's voles (Lasiopodomys brandtii) were gestated and reared to weaning under either a short (SD, 8 h:16 h L:D) or a long photoperiod (LD, 16 h:8 h L:D) at a constant ambient temperature (23°C). At weaning, male juveniles were either maintained in their initial photoperiod or transferred to the alternative photoperiod for 8 weeks. Postweaning SD voles had a lower body mass but higher thermogenic capacity compared with LD voles. At the same time, preweaning photoperiod conditions had long-lasting effects on thermogenic capacity later in life. Serum leptin concentration was positively correlated with body mass and body fat mass, whereas it was negatively correlated with energy intake and uncoupling protein 1 content in brown adipose tissue. Our results suggest that postweaning development in terms of body mass and thermogenesis is predominantly influenced by the postweaning photoperiod, while the preweaning photoperiod experience could chronically modify thermogenesis but not body mass. Furthermore, serum leptin,acting as a potential adipostatic signal, may be involved in the regulation of both energy intake and energy expenditure.

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Non‐shivering Thermogenesis and Its Thermoregulatory Significance

Cited by 561 publications

References 160 publications

Mitochondrial uncoupling prevents cold-induced oxidative stress: a case study using UCP1 knock-out mice

Mitochondrial uncoupling prevents cold-induced oxidative stress: a case study using UCP1 knock-out mice

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

Effects of photoperiod history on body mass and energy metabolism in Brandt's voles (Lasiopodomys brandtii)

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