Mammalian hibernation

In mammalian hibernation, the body temperature approaches that of the surroundings, allowing large savings in energy costs of basal metabolism and eliminating the need for heat production to compensate for heat loss. During entry into hibernation, heat production ceases while the body temperature set-point gradually decreases during slow-wave sleep. In the hibernating phase, the animal copes with problems concerning the maintenance of ion gradients, possible membrane phase transitions and the risk of ventricular fibrillation. In the arousal phase, the main part of the heat and practically all the necessary substrate comes from brown adipose tissue. The hibernation season is preceded by a preparatory phase. It may be concluded that hibernation is a practical, and perhaps even enviable, solution to a mammalian problem.

2020 ◽  
Author(s):  
Yuki Oiwa ◽  
Kaori Oka ◽  
Hironobu Yasui ◽  
Kei Higashikawa ◽  
Hidemasa Bono ◽  
...  

AbstractThe naked mole-rat (NMR) is a poikilothermic mammal that forms eusocial colonies consisting of one breeding queen, several breeding kings, and subordinates. Despite their poikilothermic feature, NMRs possess brown adipose tissue (BAT), which in homeothermic mammals induces thermogenesis in cold environments. However, NMR-BAT thermogenic potential is controversial, and its physiological roles are unknown. Here, we show that NMR-BAT has beta-3 adrenergic receptor (ADRB3)-dependent thermogenic potential, which contributes to thermogenesis in the isolated queen in non-cold environments. NMR-BAT expressed several brown adipocyte marker genes and showed noradrenaline-dependent thermogenic activity in vitro and in vivo. Although our ADRB3 inhibition experiments revealed that NMR-BAT thermogenesis slightly delays the decrease in body temperature in a cold environment, it was insufficient to maintain the body temperatures of the NMRs. In a non-cold environment, NMRs are known to increase their body temperature by a heat-sharing behavior. Interestingly, we found that the body temperatures of NMRs isolated from the colony were also significantly higher than the ambient temperature. We also show that queens, but not subordinates, induce BAT thermogenesis in isolated, non-cold conditions. Our research provides novel insights into the role and mechanism of thermoregulation in this unique poikilothermic mammal.


1965 ◽  
Vol 20 (3) ◽  
pp. 405-410 ◽  
Author(s):  
Hermann Pohl

Characteristics of cold acclimation in the golden hamster, Mesocricetus auratus, were 1) higher metabolic rate at -30 C, 2) less shivering when related to ambient temperature or oxygen consumption, and 3) higher differences in body temperature between cardiac area and thoracic subcutaneous tissues at all ambient temperatures tested, indicating changes in tissue insulation. Cold-acclimated hamsters also showed a rise in temperature of the cardiac area when ambient temperature was below 15 C. Changes in heat distribution in cold-acclimated hamsters suggest higher blood flow and heat production in the thoracic part of the body in the cold. The thermal conductance through the thoracic and lumbar muscle areas, however, did not change notably with lowering ambient temperature. Marked differences in thermoregulatory response to cold after cold acclimation were found between two species, the golden hamster and the thirteen-lined ground squirrel, showing greater ability to regulate body temperature in the cold in hamsters. hibernator; oxygen consumption— heat production; body temperature — heat conductance; muscular activity — shivering; thermoregulation Submitted on July 6, 1964


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yuki Oiwa ◽  
Kaori Oka ◽  
Hironobu Yasui ◽  
Kei Higashikawa ◽  
Hidemasa Bono ◽  
...  

Abstract The naked mole-rat (NMR) is a heterothermic mammal that forms eusocial colonies consisting of one reproductive female (queen), several reproductive males, and subordinates. Despite their heterothermy, NMRs possess brown adipose tissue (BAT), which generally induces thermogenesis in cold and some non-cold environments. Previous studies suggest that NMR-BAT induces thermogenesis by cold exposure. However, detailed NMR-BAT characteristics and whether NMR-BAT thermogenesis occurs in non-cold environments are unknown. Here, we show beta-3 adrenergic receptor (ADRB3)-dependent thermogenic potential of NMR-BAT, which contributes to thermogenesis in the isolated queen in non-cold environments (30 °C). NMR-BAT expressed several brown adipocyte marker genes and showed noradrenaline-dependent thermogenic activity in vitro and in vivo. Although our ADRB3 inhibition experiments revealed that NMR-BAT thermogenesis slightly delays the decrease in body temperature in a cold environment (20 °C), it was insufficient to prevent the decrease in the body temperatures. Even at 30 °C, NMRs are known to prevent the decrease of and maintain their body temperature by heat-sharing behaviors within the colony. However, isolated NMRs maintained their body temperature at the same level as when they are in the colony. Interestingly, we found that queens, but not subordinates, induce BAT thermogenesis in this condition. Our research provides novel insights into NMR thermoregulation.


2015 ◽  
Vol 119 (12) ◽  
pp. 1400-1410 ◽  
Author(s):  
Yeonjoo Yoo ◽  
Michelle LaPradd ◽  
Hannah Kline ◽  
Maria V. Zaretskaia ◽  
Abolhassan Behrouzvaziri ◽  
...  

The importance of exercise is increasingly emphasized for maintaining health. However, exercise itself can pose threats to health such as the development of exertional heat shock in warm environments. Therefore, it is important to understand how the thermoregulation system adjusts during exercise and how alterations of this can contribute to heat stroke. To explore this we measured the core body temperature of rats ( Tc) running for 15 min on a treadmill at various speeds in two ambient temperatures ( Ta = 25°C and 32°C). We assimilated the experimental data into a mathematical model that describes temperature changes in two compartments of the body, representing the muscles and the core. In our model the core body generates heat to maintain normal body temperature, and dissipates it into the environment. The muscles produce additional heat during exercise. According to the estimation of model parameters, at Ta = 25°C, the heat generation in the core was progressively reduced with the increase of the treadmill speed to compensate for a progressive increase in heat production by the muscles. This compensation was ineffective at Ta = 32°C, which resulted in an increased rate of heat accumulation with increasing speed, as opposed to the Ta = 25°C case. Interestingly, placing an animal on a treadmill increased heat production in the muscles even when the treadmill speed was zero. Quantitatively, this “ready-to-run” phenomenon accounted for over half of the heat generation in the muscles observed at maximal treadmill speed. We speculate that this anticipatory response utilizes stress-related circuitry.


2018 ◽  
Vol 238 (1) ◽  
pp. R53-R62 ◽  
Author(s):  
Michael E Symonds ◽  
Peter Aldiss ◽  
Neele Dellschaft ◽  
James Law ◽  
Hernan P Fainberg ◽  
...  

Although brown adipose tissue (BAT) is one of the smallest organs in the body, it has the potential to have a substantial impact on both heat production as well as fat and carbohydrate metabolism. This is most apparent at birth, which is characterised with the rapid appearance and activation of the BAT specific mitochondrial uncoupling protein (UCP)1 in many large mammals. The amount of brown fat then gradually declines with age, an adaptation that can be modulated by the thermal environment. Given the increased incidence of maternal obesity and its potential transmission to the mother’s offspring, increasing BAT activity in the mother could be one mechanism to prevent this cycle. To date, however, all rodent studies investigating maternal obesity have been conducted at standard laboratory temperature (21°C), which represents an appreciable cold challenge. This could also explain why offspring weight is rarely increased, suggesting that future studies would benefit from being conducted at thermoneutrality (~28°C). It is also becoming apparent that each fat depot has a unique transcriptome and show different developmental pattern, which is not readily apparent macroscopically. These differences could contribute to the retention of UCP1 within the supraclavicular fat depot, the most active depot in adult humans, increasing heat production following a meal. Despite the rapid increase in publications on BAT over the past decade, the extent to which modifications in diet and/or environment can be utilised to promote its activity in the mother and/or her offspring remains to be established.


2002 ◽  
Vol 92 (4) ◽  
pp. 1684-1691 ◽  
Author(s):  
Fiona C. Baker ◽  
Helen S. Driver ◽  
Janice Paiker ◽  
Geoffrey G. Rogers ◽  
Duncan Mitchell

Body temperature and sleep change in association with increased progesterone in the luteal phase of the menstrual cycle in young women. The mechanism by which progesterone raises body temperature is not known but may involve prostaglandins, inducing a thermoregulatory adjustment similar to that of fever. Prostaglandins also are involved in sleep regulation and potentially could mediate changes in sleep during the menstrual cycle. We investigated the possible role of central prostaglandins in mediating menstrual-associated 24-h temperature and sleep changes by inhibiting prostaglandin synthesis with a therapeutic dose of the centrally acting cyclooxygenase inhibitor acetaminophen in the luteal and follicular phases of the menstrual cycle in young women. Body temperature was raised, and nocturnal amplitude was blunted, in the luteal phase compared with the follicular phase. Acetaminophen had no effect on the body temperature profile in either menstrual cycle phase. Prostaglandins, therefore, are unlikely to mediate the upward shift of body temperature in the luteal phase. Sleep changed during the menstrual cycle: on the placebo night in the luteal phase the women had less rapid eye movement sleep and more slow-wave sleep than in the follicular phase. Acetaminophen did not alter sleep architecture or subjective sleep quality. Prostaglandin inhibition with acetaminophen, therefore, had no effect on the increase in body temperature or on sleep in the midluteal phase of the menstrual cycle in young women, making it unlikely that central prostaglandin synthesis underlies these luteal events.


Physiology ◽  
2004 ◽  
Vol 19 (2) ◽  
pp. 67-74 ◽  
Author(s):  
Shaun F. Morrison

Heat production in brown adipose tissue contributes to cold defense, to stress-induced increases in body temperature, and to energy balance. Elucidating the functional organization of the central network controlling the sympathetic outflow to brown adipose tissue could provide a framework for understanding how dysregulation of thermogenesis contributes to hyperthermia and to obesity.


1911 ◽  
Vol 47 (3) ◽  
pp. 605-617 ◽  
Author(s):  
Sutherland Simpson

It is held by many that the body temperature shows certain fixed diurnal and seasonal variations which cannot be accounted for by the action of the various influences, such as muscular exercise, ingestion of food, sleep, etc., which are known to affect the rate of heat production and heat loss. These variations are believed to be associated with corresponding changes in the tissue activities, and to a large extent to be independent of environmental conditions.


2006 ◽  
Vol 100 (4) ◽  
pp. 1332-1337 ◽  
Author(s):  
John Bligh

The neural process by which it is generally supposed that the stability of the body temperature of mammals is achieved has long been sought, but it remains unresolved. One hypothesis is that, as with many engineered physical systems, there is a stable reference signal with which a signal representative of body temperature is compared. Another hypothesis is that the differing coefficients of two signals that vary with temperature changes provide the set-level determinant. These could be the activities of the “cold” and “warm” sensors in response to temperature changes. Reciprocal crossing inhibition between the cold sensor to heat production effector pathways and the warm sensor to heat loss effector pathways through the central nervous system is a likely occurrence, and it could create the null-point temperature at which neither heat production nor heat loss effectors are active. This null point would be, seemingly, the set point at which body temperature is regulated. Neither hypothesis has been validated unequivocally. Students should be aware of this uncertainty about the physiological basis of homeothermy and, indeed, of homeostasis more generally. Perhaps we should be looking for a general principle that underlies the many physical and chemical stabilities of the internal environment, rather than considering them as quite separate accomplishments.


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