scholarly journals Thermoregulatory inversion: a novel thermoregulatory paradigm

2017 ◽  
Vol 312 (5) ◽  
pp. R779-R786 ◽  
Author(s):  
Domenico Tupone ◽  
Georgina Cano ◽  
Shaun F. Morrison

To maintain core body temperature in mammals, the normal central nervous system (CNS) thermoregulatory reflex networks produce an increase in brown adipose tissue (BAT) thermogenesis in response to skin cooling and an inhibition of the sympathetic outflow to BAT during skin rewarming. In contrast, these normal thermoregulatory reflexes appear to be inverted in hibernation/torpor; thermogenesis is inhibited during exposure to a cold environment, allowing dramatic reductions in core temperature and metabolism, and thermogenesis is activated during skin rewarming, contributing to a return of normal body temperature. Here, we describe two unrelated experimental paradigms in which rats, a nonhibernating/torpid species, exhibit a “thermoregulatory inversion,” which is characterized by an inhibition of BAT thermogenesis in response to skin cooling, and a switch in the gain of the skin cooling reflex transfer function from negative to positive values. Either transection of the neuraxis immediately rostral to the dorsomedial hypothalamus in anesthetized rats or activation of A1 adenosine receptors within the CNS of free-behaving rats produces a state of thermoregulatory inversion in which skin cooling inhibits BAT thermogenesis, leading to hypothermia, and skin warming activates BAT, supporting an increase in core temperature. These results reflect the existence of a novel neural circuit that mediates inverted thermoregulatory reflexes and suggests a pharmacological mechanism through which a deeply hypothermic state can be achieved in nonhibernating/torpid mammals, possibly including humans.

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Fredrik A. F. Markussen ◽  
Vebjørn J. Melum ◽  
Béatrice Bothorel ◽  
David G. Hazlerigg ◽  
Valérie Simonneaux ◽  
...  

Abstract Background Hibernation is a physiological and behavioural adaptation that permits survival during periods of reduced food availability and extreme environmental temperatures. This is achieved through cycles of metabolic depression and reduced body temperature (torpor) and rewarming (arousal). Rewarming from torpor is achieved through the activation of brown adipose tissue (BAT) associated with a rapid increase in ventilation frequency. Here, we studied the rate of rewarming in the European hamster (Cricetus cricetus) by measuring both BAT temperature, core body temperature and ventilation frequency. Results Temperature was monitored in parallel in the BAT (IPTT tags) and peritoneal cavity (iButtons) during hibernation torpor-arousal cycling. We found that increases in brown fat temperature preceded core body temperature rises by approximately 48 min, with a maximum re-warming rate of 20.9℃*h-1. Re-warming was accompanied by a significant increase in ventilation frequency. The rate of rewarming was slowed by the presence of a spontaneous thoracic mass in one of our animals. Core body temperature re-warming was reduced by 6.2℃*h-1 and BAT rewarming by 12℃*h-1. Ventilation frequency was increased by 77% during re-warming in the affected animal compared to a healthy animal. Inspection of the position and size of the mass indicated it was obstructing the lungs and heart. Conclusions We have used a minimally invasive method to monitor BAT temperature during arousal from hibernation illustrating BAT re-warming significantly precedes core body temperature re-warming, informing future study design on arousal from hibernation. We also showed compromised re-warming from hibernation in an animal with a mass obstructing the lungs and heart, likely leading to inefficient ventilation and circulation.


2008 ◽  
Vol 109 (2) ◽  
pp. 318-338 ◽  
Author(s):  
Daniel I. Sessler ◽  
David S. Warner ◽  
Mark A. Warner

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Peng Zhou ◽  
Maricela Robles-Murguia ◽  
Deepa Mathew ◽  
Giles E. Duffield

Inhibitor of DNA binding 2 (ID2) is a helix-loop-helix transcriptional repressor rhythmically expressed in many adult tissues. Our previous studies have demonstrated thatId2null mice have sex-specific elevated glucose uptake in brown adipose tissue (BAT). Here we further explored the role ofId2in the regulation of core body temperature over the circadian cycle and the impact ofId2deficiency on genes involved in insulin signaling and adipogenesis in BAT. We discovered a reduced core body temperature inId2−/− mice. Moreover, inId2−/− BAT, 30 genes includingIrs1,PPARs, andPGC-1s were identified as differentially expressed in a sex-specific pattern. These data provide valuable insights into the impact ofId2deficiency on energy homeostasis of mice in a sex-specific manner.


2018 ◽  
Vol 315 (6) ◽  
pp. E1224-E1231 ◽  
Author(s):  
Liping Qiao ◽  
Samuel Lee ◽  
Amanda Nguyen ◽  
William W. Hay ◽  
Jianhua Shao

To determine the role of UCP1-mediated thermogenesis in controlling maternal metabolic adaptation to pregnancy, energy metabolism of C57BL/6 wild-type (WT) and Ucp1 gene knockout ( Ucp1−/−) mice was studied during pregnancy. With the progression of pregnancy, maternal energy expenditure rates (EERs), expression of UCP1, and core body temperature steadily declined in WT dams. Despite no significant alterations in core body temperature and weight gain during pregnancy, Ucp1−/− dams exhibited lower rates in EER decline. High-fat (HF) feeding not only robustly increased maternal UCP1 expression and core body temperature but also abolished gestation-suppressed EER in WT dams. However, HF-increased EERs were significantly attenuated in Ucp1−/− dams. Significantly increased fetal body weights and fetal/placental weight ratio were detected in fetuses from Ucp1−/− dams compared with fetuses from WT dams. Markedly increased expression levels of glucose transporter 1 and amino acid transporters were also observed in placentas from Ucp1−/− dams. Furthermore, blood glucose concentrations of fetuses from Ucp1−/− dams were significantly higher than those of fetuses from WT dams, indicating that maternal UCP1 has an inhibitory effect on placental efficiency and fetal growth. Taken all together, this study demonstrated that maternal brown adipose tissue plays an important role in controlling maternal metabolic adaptation and placental nutrient transport.


2017 ◽  
Vol 60 (3) ◽  
pp. 19-25
Author(s):  
Sławomir Kujawski ◽  
Joanna Słomko ◽  
Monika Zawadka-Kunikowska ◽  
Mariusz Kozakiewicz ◽  
Jacek J. Klawe ◽  
...  

Abstract Changes observed in the core body temperature of divers are the result of a multifaceted response from the body to the change of the external environment. In response to repeated activities, there may be a chronic, physiological adaptation of the body’s response system. This is observed in the physiology of experienced divers while diving. The purpose of this study is to determine the immediate and delayed effects of hyperbaric exposure on core temperature, as well as its circadian changes in a group of three experienced divers. During compression at 30 and 60 meters, deep body temperature values tended to increase. Subsequently, deep body temperature values showed a tendency to decrease during decompression. All differences in core temperature values obtained by the group of divers at individual time points in this study were not statistically significant.


2010 ◽  
Vol 299 (6) ◽  
pp. R1478-R1488 ◽  
Author(s):  
Marshall Hampton ◽  
Bethany T. Nelson ◽  
Matthew T. Andrews

Small hibernating mammals show regular oscillations in their heart rate and body temperature throughout the winter. Long periods of torpor are abruptly interrupted by arousals with heart rates that rapidly increase from 5 beats/min to over 400 beats/min and body temperatures that increase by ∼30°C only to drop back into the hypothermic torpid state within hours. Surgically implanted transmitters were used to obtain high-resolution electrocardiogram and body temperature data from hibernating thirteen-lined ground squirrels ( Spermophilus tridecemlineatus ). These data were used to construct a model of the circulatory system to gain greater understanding of these rapid and extreme changes in physiology. Our model provides estimates of metabolic rates during the torpor-arousal cycles in different model compartments that would be difficult to measure directly. In the compartment that models the more metabolically active tissues and organs (heart, brain, liver, and brown adipose tissue) the peak metabolic rate occurs at a core body temperature of 19°C approximately midway through an arousal. The peak metabolic rate of the active tissues is nine times the normothermic rate after the arousal is complete. For the overall metabolic rate in all tissues, the peak-to-resting ratio is five. This value is high for a rodent, which provides evidence for the hypothesis that the arousal from torpor is limited by the capabilities of the cardiovascular system.


2011 ◽  
Vol 46 (5) ◽  
pp. 566-573 ◽  
Author(s):  
Stephanie M. Mazerolle ◽  
Matthew S. Ganio ◽  
Douglas J. Casa ◽  
Jakob Vingren ◽  
Jennifer Klau

Context: Oral temperature might not be a valid method to assess core body temperature. However, many clinicians, including athletic trainers, use it rather than criterion standard methods, such as rectal thermometry. Objective: To critically evaluate original research addressing the validity of using oral temperature as a measurement of core body temperature during periods of rest and changing core temperature. Data Sources: In July 2010, we searched the electronic databases PubMed, Scopus, Cumulative Index to Nursing and Allied Health Literature (CINAHL), SPORTDiscus, Academic Search Premier, and the Cochrane Library for the following concepts: core body temperature, oral, and thermometers. Controlled vocabulary was used, when available, as well as key words and variations of those key words. The search was limited to articles focusing on temperature readings and studies involving human participants. Data Synthesis: Original research was reviewed using the Physiotherapy Evidence Database (PEDro). Sixteen studies met the inclusion criteria and subsequently were evaluated by 2 independent reviewers. All 16 were included in the review because they met the minimal PEDro score of 4 points (of 10 possible points), with all but 2 scoring 5 points. A critical review of these studies indicated a disparity between oral and criterion standard temperature methods (eg, rectal and esophageal) specifically as the temperature increased. The difference was −0.50°C ± 0.31°C at rest and −0.58°C ± 0.75°C during a nonsteady state. Conclusions: Evidence suggests that, regardless of whether the assessment is recorded at rest or during periods of changing core temperature, oral temperature is an unsuitable diagnostic tool for determining body temperature because many measures demonstrated differences greater than the predetermined validity threshold of 0.27°C (0.5°F). In addition, the differences were greatest at the highest rectal temperatures. Oral temperature cannot accurately reflect core body temperature, probably because it is influenced by factors such as ambient air temperature, probe placement, and ingestion of fluids. Any reliance on oral temperature in an emergency, such as exertional heat stroke, might grossly underestimate temperature and delay proper diagnosis and treatment.


2021 ◽  
Author(s):  
Marta Lantero Rodriguez ◽  
Maaike Schilperoort ◽  
Inger Johansson ◽  
Elin Svedlund Eriksson ◽  
Vilborg Palsdottir ◽  
...  

Brown adipose tissue (BAT) burns substantial amounts of mainly lipids to produce heat. Some studies indicate that BAT activity and core body temperature are lower in males than females. Here we investigated the role of testosterone and its receptor (the androgen receptor; AR) in metabolic BAT activity in male mice. Castration, which renders mice testosterone deficient, slightly promoted the expression of thermogenic markers in BAT, decreased BAT lipid content, and increased basal lipolysis in isolated brown adipocytes. Further, castration increased the core body temperature. Triglyceride-derived fatty acid uptake, a proxy for metabolic BAT activity in vivo, was strongly increased in BAT from castrated mice (4.5-fold increase vs. sham-castrated mice) and testosterone replacement reversed the castration-induced increase in metabolic BAT activity. BAT-specific AR deficiency did not mimic the castration effects in vivo and AR agonist treatment did not diminish the activity of cultured brown adipocytes in vitro, suggesting that androgens do not modulate BAT activity via a direct, AR-mediated pathway. In conclusion, testosterone is a negative regulator of metabolic BAT activity in male mice. Our findings provide new insight into the metabolic actions of testosterone.


2019 ◽  
Vol 91 (2) ◽  
pp. 25-29
Author(s):  
Paweł Podsiadło ◽  
Sylweriusz Kosiński ◽  
Tomasz Darocha ◽  
Katherine Zerebiec ◽  
Przemysław Wolak ◽  
...  

Background: An unintentional drop in core body temperature of trauma victims is associated with increased mortality. Thermoregulation is impaired in these patients, especially when treated with opioids or anesthetics. Careful thermal insulation and active warming are necessary to maintain normothermia. The aim of the study was to assess the equipment and procedures for diagnosing and managing post-traumatic hypothermia in Polish hospitals. Methods: Survey forms regarding equipment and procedures on monitoring of core temperature (Tc) and active warming were distributed to every hospital that admits trauma victims in the Holy Cross Province. Questionnaires were addressed to surgery departments, intensive care units (ICUs) and operating rooms (ORs). Results: 92% of surgery departments did not have equipment to measure core body temperature and 85% did not have equipment to rewarm patients. Every ICU had equipment to measure Tc and 83% had active warming devices. In 50% of ICUs, there were no rewarming protocols based on Tc and the initiation of rewarming was left to the physician’s discretion. In 58% of ORs Tc was not monitored and in 33% the patients were not actively warmed. Conclusions: The majority of surveyed ICUs and ORs are adequately equipped to identify and treat hypothermia, however the criteria for initiating Tc monitoring and rewarming remain unstandardized. Surgery departments are not prepared to manage post-traumatic hypothermia.


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