Maintenance Of Body Temperature Research Articles

Brown adipose tissue facilitates the fever response following infection with Salmonella enterica serovar Typhimurium in mice

Brown adipose tissue (BAT) combusts lipids and glucose to generate heat. Via this process of nonshivering thermogenesis, BAT plays a pivotal role in thermoregulation in cold environments, but its contribution to immune-induced fever is less clear. Male APOE∗3-Leiden.CETP mice, a well-established model for human-like lipoprotein metabolism, and wild-type mice were given an intraperitoneal injection of Salmonella enterica serovar Typhimurium (S.tm). Energy expenditure and substrate utilization, plasma lipid levels, fatty acid (FA) uptake by adipose tissues, and lipid content and thermogenic markers in adipose tissues were examined. S.tm infection led to a set of characteristic symptoms, including elevated body temperature and decreased body weight. Whole-body energy expenditure was significantly decreased 72 h postinfection, but fat oxidation was increased and accompanied by a substantial reduction in plasma triglyceride (TG) levels as demonstrated in APOE∗3-Leiden.CETP mice. S.tm infection strongly increased uptake of FAs from TG-rich lipoproteins by BAT, which showed a positive correlation with body temperature in infected mice. Upon histological examination of BAT from wild-type or APOE∗3-Leiden.CETP mice, elevated levels of tyrosine hydroxylase were observed, indicative of stimulated sympathetic activity. In addition, the gene expression profile was consistent with more adrenergic stimulation, while lipid content was reduced. Furthermore, browning of white adipose tissue was observed, evidenced by a modest increase in TG-derived FA uptake, the presence of multilocular cells, and induction of uncoupling protein 1 expression. We proposed that BAT, or thermogenic adipose tissue in general, is involved in the maintenance of elevated body temperature upon invasive bacterial infection.

Revolutionizing trauma care: advancing coagulation management and damage control anesthesia.

Despite advances in emergency transfer systems and trauma medicine, the incidence of preventable deaths due to massive hemorrhage remains high. Recent immunological research has elucidated key mechanisms underlying trauma-induced coagulopathy in the early stages of trauma, including sympathoadrenal stimulation, shedding of the glycocalyx, and endotheliopathy. Consequently, the condition progresses to fibrinogen depletion, hyperfibrinolysis, and platelet dysfunction. Coexisting factors such as uncorrected acidosis, hypothermia, excessive crystalloid administration, and a history of anticoagulant use exacerbate coagulopathy. This study introduces damage-control anesthetic management based on recent insights into damage-control resuscitation, emphasizing the importance of rapid transport, timely bleeding control, early administration of antifibrinolytics and fibrinogen concentrates, and maintenance of calcium levels and body temperature. Additionally, this study discusses brain-protective strategies for trauma patients with brain injuries and the utilization of cartridge-based viscoelastic assays for goal-directed coagulation management in trauma settings. This comprehensive approach may provide potential insights for anesthetic management in the fast-paced field of trauma medicine.

Here comes the sun: Thermoregulatory behavior in ectotherms illuminated by light‐level geolocators

AbstractDaily activity patterns of free‐ranging wildlife affect a wide range of ecological and physiological processes and, in turn are affected by anthropogenic disturbances to the environment. However, obtaining a continuous record of activity without disturbing wild animals is logistically challenging. We used commercially available, multi‐purpose light‐level geolocator dataloggers to continuously record light environment and time spent out of water during 5‐months (1 May to 9 September 2021) in an ectothermic freshwater turtle species, the northern map turtle (Graptemys geographica). We used these data to compare time of year and sex differences in thermoregulatory behavior in an ectothermic species in its natural habitat. We recorded >500 000 data points from 17 individual turtles (nine males and eight females). We found no differences in the mean light levels, or proportion of time spent out of the water, between males and females. However, there was a significant effect of both time of year and sex by time of year interaction in both light level, proportion of time spent dry, and number of state changes (i.e., shuttling behavior, wet to dry or dry to wet), suggesting that turtles alter their aerial basking behavior over the course of the season and that the changes in patterns of aerial basking behavior differ between the sexes throughout the year. In general, the proportion of time spent dry decreased over the active season, with an increase during the last week of June and the first week of July, while the number of state changes increased in females during late May/early June before decreasing, while males remained relatively constant. These changes may reflect the different energetic demands associated with reproduction between the two sexes. The overall downward trend in aerial basking likely reflects the role of increasing environmental temperatures, particularly water temperature, in the maintenance of body temperature in this largely aquatic species.

Regulation of Neural Functions byBrain Temperature and Thermo-TRP Channels.

Body temperature is an important determinant in regulating the activities of animals. In humans, a mild 0.5°C hyperthermia can cause headaches, demonstrating that the maintenance of normal body temperature is a key for our health. In a more extreme example, accidental acute hypothermia can lead to severe shivering, loss of consciousness, or death, although the details of these mechanisms are poorly understood. We previously found that the TRPV4 ion channel is constitutively activated by normal body temperature. The activation threshold of TRPV4 is >34°C in the brain, which enables TRPV4 to convert thermal information into cellular signaling. Here we review the data that describe how the deletion of TRPV4 evokes abnormal behavior in mice. These studies demonstrate that the maintenance of body temperature and the sensory system for detecting body temperature, such as via TRPV4, are critical components for normal cellular function. Moreover, abnormal TRPV4 activation exacerbates cell death, epilepsy, stroke, or brain edema. Notably, TRPV4 can detect mechanical stimuli and contributes to various neural functions similar to the mechanosensitive characteristics of TRPV2. In this review, I summarize the findings related to TRPV2/TRPV4 and neural functions.

Similarities and differences regarding acute anorexia nervosa and semi-starvation: does behavioral thermoregulation play a central role?

To clarify the association between acute anorexia nervosa (AN) and semi-starvation (SS) by focusing on similarities and differences in physiology, mood, and behavior. A comparison of published literature between these two groups. Both groups show similar hormonal and metabolic changes in response to caloric restriction and extreme weight loss (~25%). Associated changes result in a reduced body temperature (Tcore-low). Maintenance of body temperature within a specific range is crucial to survival. However, both groups cannot activate autonomic strategies to maintain their Tcore-low, such as increasing metabolic rate, constricting skin blood vessels, or shivering. Furthermore, Tcore-low increases the individuals' "coldness sensations" throughout the body, hence the frequent reports from ANs and SSs of "feeling cold." To eliminate these uncomfortable "coldness sensations" and, importantly, to maintain Tcore-low, ANs, and SSs "select" different thermoregulatory behavioral strategies. It is proposed that the primary differences between AN and SS, based on genetics, now manifest due to the "selection" of different thermo-regulatory behaviors. AN patients (ANs) "select" hyperactive behavior (HyAc), which increases internal metabolic heat and thus assists with maintaining Tcore-low; in harmony with hyperactive behavior is a lively mood. Also related to this elevated arousal pattern, ANs experience disrupted sleep. In contrast, SS individuals "select" a passive thermo-behavioral strategy, "shallow torpor," which includes reduced activity, resulting in energy conservation. In addition, this inactivity aids in the retention of generated metabolic heat. Corresponding to this lethargic behavior, SS individuals display a listless mood and increased sleep. Initial similarities between the two are attributable to physiological changes related to extreme weight loss. Differences are most likely attributable to genetically programmed "selection" of alternate thermoregulatory strategies, primarily to maintain Tcore-low. However, if acute AN is prolonged and evolves into a chronic condition, AN will more closely align with starvation and more precisely reflect SS symptomology.

The multifaceted role of macrophages in homeostatic and injured skeletal muscle.

Skeletal muscle is essential for body physical activity, energy metabolism, and temperature maintenance. It has excellent capabilities to maintain homeostasis and to regenerate after injury, which indispensably relies on muscle stem cells, satellite cells (MuSCs). The quiescence, activation, and differentiation of MuSCs are tightly regulated in homeostatic and regenerating muscles. Among the important regulators are intramuscular macrophages, which are functionally heterogeneous with different subtypes present in a spatiotemporal manner to regulate the balance of different MuSC statuses. During chronic injury and aging, intramuscular macrophages often undergo aberrant activation, which in turn disrupts muscle homeostasis and regenerative repair. Growing evidence suggests that the aberrant activation is mainly triggered by altered muscle microenvironment. The trained immunity that affects myeloid progenitors during hematopoiesis may also contribute. Aged immune system may contribute, in part, to the aging-related sarcopenia and compromised skeletal muscle injury repair. As macrophages are actively involved in the progression of many muscle diseases, manipulating their functional activation has become a promising therapeutic approach, which requires comprehensive knowledge of the cellular and molecular mechanisms underlying the diverse activation. To this end, we discuss here the current knowledge of multifaceted role of macrophages in skeletal muscle homeostasis, injury, and repair.

A review on active heating for high performance cold-proof clothing

PurposeThe present study provides a comprehensive review of the advancements in five active heating modes for cold-proof clothing as of 2021. It aims to evaluate the current state of research for each heating mode and identify their limitations. Further, the study provides insights into the optimization of intelligent temperature control algorithms and design considerations for intelligent cold-proof clothing.Design/methodology/approachThis article presents a classification of active heating systems based on five different heating principles: electric heating system, solar heating system, phase-change material (PCM) heating system, chemical heating system and fluid/air heating system. The systems are analyzed and evaluated in terms of heating principle, research advancement, scientific challenges and application potential in the field of cold-proof clothing.FindingsThe rational utilization of active heating modes enhances the thermal efficiency of cold-proof clothing, resulting in enhanced cold-resistance and reduced volume and weight. Despite progress in the development of the five prevalent heating modes, particularly with regard to the improvement and advancement of heating materials, the current integration of heating systems with cold-proof clothing is limited to the torso and limbs, lacking consideration of the thermal physiological requirements of the human body. Additionally, the heating modes of each system tend to be uniform and lack differentiation to meet the varying cold protection needs of various body parts.Research limitations/implicationsThe effective application of multiple heating modes helps the human body to maintain a constant body temperature and thermal equilibrium in a cold environment. The research of heating mode is the basis for realizing the temperature control of cold-proof clothing and provides an effective guarantee for the future development of the intelligent algorithms for temperature control of non-uniform heating of body segments.Practical implicationsThe integration of multiple heating modes ensures the maintenance of a constant body temperature and thermal balance for the wearer in cold environments. The research of heating modes forms the foundation for the temperature regulation of cold-proof clothing and lays the groundwork for the development of intelligent algorithms for non-uniform heating control of different body segments.Originality/valueThe present article systematically reviews five active heating modes suitable for use in cold-proof clothing and offers guidance for the selection of heating systems in future smart cold-proof clothing. Furthermore, the findings of this research provide a basis for future research on non-uniform heating modes that are aligned with the thermal physiological needs of the human body, thus contributing to the development of cold-proof clothing that is better suited to meet the thermal needs of the human body.

Linking Hypothermia and Altered Metabolism with TrkB Activation.

Many mechanisms have been proposed to explain acute antidepressant drug-induced activation of TrkB neurotrophin receptors, but several questions remain. In a series of pharmacological experiments, we observed that TrkB activation induced by antidepressants and several other drugs correlated with sedation, and most importantly, coinciding hypothermia. Untargeted metabolomics of pharmacologically dissimilar TrkB activating treatments revealed effects on shared bioenergetic targets involved in adenosine triphosphate (ATP) breakdown and synthesis, demonstrating a common perturbation in metabolic activity. Both activation of TrkB signaling and hypothermia were recapitulated by administration of inhibitors of glucose and lipid metabolism, supporting a close relationship between metabolic inhibition and neurotrophic signaling. Drug-induced TrkB phosphorylation was independent of electroencephalography slow-wave activity and remained unaltered in knock-in mice with the brain-derived neurotrophic factor (BDNF) Val66Met allele, which have impaired activity-dependent BDNF release, alluding to an activation mechanism independent from BDNF and neuronal activity. Instead, we demonstrated that the active maintenance of body temperature prevents activation of TrkB and other targets associated with antidepressants, including p70S6 kinase downstream of the mammalian target of rapamycin (mTOR) and glycogen synthase kinase 3β (GSK3β). Increased TrkB, GSK3β, and p70S6K phosphorylation was also observed during recovery sleep following sleep deprivation, when a physiological temperature drop is known to occur. Our results suggest that the changes in bioenergetics and thermoregulation are causally connected to TrkB activation and may act as physiological regulators of signaling processes involved in neuronal plasticity.

Mammalian maxilloturbinal evolution does not reflect thermal biology

The evolution of endothermy in vertebrates is a major research topic in recent decades that has been tackled by a myriad of research disciplines including paleontology, anatomy, physiology, evolutionary and developmental biology. The ability of most mammals to maintain a relatively constant and high body temperature is considered a key adaptation, enabling them to successfully colonize new habitats and harsh environments. It has been proposed that in mammals the anterior nasal cavity, which houses the maxilloturbinal, plays a pivotal role in body temperature maintenance, via a bony system supporting an epithelium involved in heat and moisture conservation. The presence and the relative size of the maxilloturbinal has been proposed to reflect the endothermic conditions and basal metabolic rate in extinct vertebrates. We show that there is no evidence to relate the origin of endothermy and the development of some turbinal bones by using a comprehensive dataset of µCT-derived maxilloturbinals spanning most mammalian orders. Indeed, we demonstrate that neither corrected basal metabolic rate nor body temperature significantly correlate with the relative surface area of the maxilloturbinal. Instead, we identify important variations in the relative surface area, morpho-anatomy, and complexity of the maxilloturbinal across the mammalian phylogeny and species ecology.

The muscle-enriched myokine Musclin impairs beige fat thermogenesis and systemic energy homeostasis via Tfr1/PKA signaling in male mice

Skeletal muscle and thermogenic adipose tissue are both critical for the maintenance of body temperature in mammals. However, whether these two tissues are interconnected to modulate thermogenesis and metabolic homeostasis in response to thermal stress remains inconclusive. Here, we report that human and mouse obesity is associated with elevated Musclin levels in both muscle and circulation. Intriguingly, muscle expression of Musclin is markedly increased or decreased when the male mice are housed in thermoneutral or chronic cool conditions, respectively. Beige fat is then identified as the primary site of Musclin action. Muscle-transgenic or AAV-mediated overexpression of Musclin attenuates beige fat thermogenesis, thereby exacerbating diet-induced obesity and metabolic disorders in male mice. Conversely, Musclin inactivation by muscle-specific ablation or neutralizing antibody treatment promotes beige fat thermogenesis and improves metabolic homeostasis in male mice. Mechanistically, Musclin binds to transferrin receptor 1 (Tfr1) and antagonizes Tfr1-mediated cAMP/PKA-dependent thermogenic induction in beige adipocytes. This work defines the temperature-sensitive myokine Musclin as a negative regulator of adipose thermogenesis that exacerbates the deterioration of metabolic health in obese male mice and thus provides a framework for the therapeutic targeting of this endocrine pathway.

Participation of blood valine and L-arginine-NO system in the development of hyperthermia, the formation of thyroid status and prooxidant-antioxidant state under stress due to bacterial endotoxin

The importance of free amino acids in the processes of vital activity in normal and pathological conditions is well known. At the same time, there are no data on the role of blood plasma valine in the formation of thyroid status, prooxidant-antioxidant state, and in the development of hyperthermia caused by bacterial endotoxin, although its participation in these processes is quite natural, since valine is an inhibitor of arginase, the activity of which affects the level of arginine amino acid and nitric monoxide (NO). This is important in the regulation of body temperature, lipidperoxidation processes, and the level of iodine-containing hormones. The aim of the study was to elucidate the significance of blood plasma valine and the L-arginine-NO system in the formation of thyroid status, prooxidant-antioxidant state and the maintenance of body temperature during stress caused by bacterial endotoxin. In experiments on rats and rabbits, it was found that under the conditions of E. сoli lipopolysaccharide action in the body of animals, the pituitary-thyroid gland system, lipid peroxidation (LPO) processes in the blood and liver activate, the nitrate/nitrite (NO3–/NO2–) content increases, the level of valine and arginine in the blood plasma decreases, and body temperature increases . Under the conditions of depression of liver arginase with L- valine (100 mg / kg intraperitoneally 30 minutes before endotoxin injection ), the LPS action is not accompanied by an increase in body temperature , leads to less pronounced changes in lipid peroxidation processes , as well as to a more significant decrease in the triiodothyronine content and to an increase in the NO3–/NO2– level in blood plasma in rats . Preliminary administration of the NO synthesis inhibitor L-NAME (25 mg / kg intraperitoneally 30 minutes before endotoxin injection ) into the animal body not only reduces body temperature rise and NO3–/NO2– level increase in the blood plasma when acted upon by endotoxin , but also exacerbates changes in the LPO processes in the blood plasma and liver , and prevents the activation of the pituitary-thyroid gland system .

Effects of Forced-Air Warming Therapy on Anxiety, Pain, and Body Temperature of Patients under Local Anesthesia during Surgery: A Quasi-Experimental Study

Purpose: This study aimed to evaluate the effect of forced air-warming therapy on anxiety, pain, and body temperature maintenance for local anesthesia patients.Methods: The study had a nonequivalent control group, pretest-posttest design. The participants were 70 patients undergoing local anesthesia (35 in the experimental group and 35 in the control group) at a tertiary general hospital. The participants in the experimental group were provided forced air-warming blankets, and the control group was given available blankets. Data were collected from May 1 to July 31, 2020, and analyzed using SPSS/WIN 27.0, the independent t-test, Repeated Measures ANOVA, Repeated Measures ANCOVA, and the Bonferroni correction.Results: Postoperative state anxiety and pain scores significantly differed over time between the experimental and control groups. Postoperative body temperatures were also significantly different between the groups and over time.Conclusion: Applyinga forced air-warming blanket is an effective nursing intervention toreduce anxiety and pain, and increase the body temperature of patients under local anesthesia during surgery. Therefore, forced air-warming blankets should be actively used for those patients.

Hyperthermia alters neurobehavior by affecting cell proliferation and neuronal survival in young male rats

Maintenance of body temperature within physiological range is critical for the fetal and neonatal development. Hyperthermia is one of the most frequently encountered pediatric complaints and may cause neurological disorders due to neuronal injury. In this study, we aimed to investigate the effects of hyperthermia on behavioral alterations, neuronal survival, apoptosis, and cell proliferation in young male Sprague-Dawley rats. Twenty-one 13-day-old rats were randomly divided into three groups (n = 7 per group). Body temperature was increased to 39°C and 41°C in a hyperthermia induction chamber for 30 min, whereas the animals in control group were maintained at 36°C. Twenty-four hours after hyperthermia, animals were subjected to the open field test, elevated-O-maze test, and grip strength test to assess the locomotor activity, anxiety, and motor function. Neuronal survival, apoptosis, and cell proliferation were investigated in cortex, hippocampal dentate gyrus (DG) and CA1 regions, and corpus callosum (CC). Decreased locomotor activity and motor function and increased anxiety were observed in the hyperthermia groups, and these were more pronounced in the 41°C group. Neuronal survival was significantly decreased in DG, CA1, and CC in the hyperthermia groups (**p < 0.01). Apoptosis was significantly induced in cortex, DG, and CC of the animals exposed to heat (*p < 0.05). In addition, cell proliferation positivity decreased significantly only in DG and CC of the animals exposed to heat (*p < 0.05). Our results suggest that neurobehavioral deficits caused by hyperthermia may be due to the increased apoptosis and neuronal cell death and decreased cell proliferation in the brain of postnatal developing rats.

Abstract 4836: Fasting induces greater expression of mitochondrial proteins associated with fatty acid metabolism and non-shivering thermogenesis in brown adipose tissue of knock-in ACSS1K635Q mice

Abstract Introduction: Acyl-CoA Synthetase Short Chain Family Member 1 (ACSS1) is an important mitochondrial enzyme for the production of ATP from short chain fatty acids under energetic stress. ACSS1 is highly expressed in brown adipose tissue, heart, and skeletal muscle. ACSS1 is regulated in part by a post-translational modification of ACSS1, whereby the side chain of Lysine-635 is acetylated. The activity of ACSS1 is downregulated by the acetylation of Lysine-635. The downregulation of ACSS1 activity has been shown to impose changes on fatty acid metabolism and body temperature. Our lab observed that homozygous knock-in ACSS1 mice that fasted for 48 hours were hypothermic with a temperature of 30 °C. Here, we utilized mutant mice to simulate acetylated ACSS1, to investigate the role of ACSS1K635Q in mitochondrial fatty acid metabolism and maintenance of body temperature under fasting conditions. Methods: A knock-in ACSS1 mouse model with a mutation of ACSS1K635Q was designed to model the downregulation of ACSS1. Wild Type mice and Homozygous Knock-in ACSS1K635Q mice were either fasted for 48 hours (F48) or fed with a normal diet (ND). Four experimental groups - Wild Type ND and F48 mice and Homozygous Knock-in ACSS1K635Q ND and F48 mice - were examined. Protein was extracted from 10 samples each containing 20 mg of brown adipose tissue. Tissue samples were lysed and immunoblotted with primary and secondary antibodies. Western Blot Western Blot was performed on the proteins Uncoupling Protein 1 (UCP1), UCP2, ACC, and AMPK. Membranes were imaged using the FluorChem M system, and chemiluminescence was quantified using the NIH ImageJ software. ANOVA and t-test were used to conduct statistical analysis (P &amp;lt; 0.05). Results: Homozygous Ki-ACSS1K635Q F48 mice expressed higher levels of UCP1 and UCP2 in BAT than Homozygous Ki-ACSS1K635Q ND mice. We observed a greater difference in UCP1 expression between Homozygous Ki-CSS1K635Q ND and F48 mice compared to the difference in UCP1 expression between Wild Type ND and F48 mice. In Wild Type and Homozygous Ki-ACSS1K635Q mice, UCP1 expression was lower than UCP2 expression. Fasting for 48 hours significantly upregulated p-AMPK in Wild Type mice. Conclusions: Under fasting conditions, metabolic processes may shift towards a greater proportion of non-shivering thermogenesis due to ACSS1 inactivity. UCP1 likely contributes more to non-shivering thermogenesis than UCP2. Understanding the impact of acetylating ACSS1 provides avenues towards developing personalized treatments that effectively respond to metabolic stressors. Citation Format: Aishani Sivasai Gargapati, Mahboubeh Varmazyad, David Gius. Fasting induces greater expression of mitochondrial proteins associated with fatty acid metabolism and non-shivering thermogenesis in brown adipose tissue of knock-in ACSS1K635Q mice. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4836.

Sex differences in thermoregulation in mammals: Implications for energy homeostasis.

Thermal homeostasis is a fundamental process in mammals, which allows the maintenance of a constant internal body temperature to ensure an efficient function of cells despite changes in ambient temperature. Increasing evidence has revealed the great impact of thermoregulation on energy homeostasis. Homeothermy requires a fine regulation of food intake, heat production, conservation and dissipation and energy expenditure. A great interest on this field of research has re-emerged following the discovery of thermogenic brown adipose tissue and browning of white fat in adult humans, with a potential clinical relevance on obesity and metabolic comorbidities. However, most of our knowledge comes from male animal models or men, which introduces unwanted biases on the findings. In this review, we discuss how differences in sex-dependent characteristics (anthropometry, body composition, hormonal regulation, and other sexual factors) influence numerous aspects of thermal regulation, which impact on energy homeostasis. Individuals of both sexes should be used in the experimental paradigms, considering the ovarian cycles and sexual hormonal regulation as influential factors in these studies. Only by collecting data in both sexes on molecular, functional, and clinical aspects, we will be able to establish in a rigorous way the real impact of thermoregulation on energy homeostasis, opening new avenues in the understanding and treatment of obesity and metabolic associated diseases.

Energetic costs of bill heat exchange demonstrate contributions to thermoregulation at high temperatures in toco toucans (Ramphastos toco).

Body temperature regulation under changes in ambient temperature involves adjustments in heat production and heat exchange rates between the animal and the environment. One mechanism involves the modulation of the surface temperature of specific areas of the body through vasomotor adjustment. In homeotherms, this thermoregulatory adjustment is essential for the maintenance of body temperature over a moderate temperature range, known as the thermal neutral zone (TNZ). The bill of the toco toucan (Ramphastos toco) has been described as a highly efficient thermal window and hypothesized to assist in the thermal homeostasis of this bird. Herein, we directly evaluated the contribution of heat exchange through the bill of the toco toucan and role of the bill in the delimitation of the TNZ. To do this, we measured metabolic rate (MR), via oxygen consumption, over a range of ambient temperatures from 0 to 35°C. MR measurements were made in birds with the bill intact and with the bill insulated. The limits of the TNZ did not differ between treatments, ranging from 10.8 to 25.0°C. The MR differed among treatments only at elevated temperatures (30 and 35°C), reaching 0.92±0.11ml O2g-1h-1 (mean±s.d.) for the intact group and 1.13±0.13ml O2g-1h-1 for the insulated group. These results indicate that although heat dissipation through the bill does not contribute significantly to widening of the TNZ, it may well be critically important in assisting body temperature regulation at higher temperatures extending above the upper limit of the TNZ.

Rats lacking Ucp1 present a novel translational tool for the investigation of thermogenic adaptation during cold challenge.

Valuable studies have tested the role of UCP1 on body temperature maintenance in mice, and we sought to knockout Ucp1 in rats (Ucp1-/- ) to provide insight into thermogenic mechanisms in larger mammals. We used CRISPR/Cas9 technology to create Ucp1-/- rats. Body weight and adiposity were measured, and rats were subjected to indirect calorimetry. Rats were maintained at room temperature or exposed to 4°C for either 24 h or 14 days. Analyses of brown and white adipose tissue and skeletal muscle were conducted via histology, western blot comparison of oxidative phosphorylation proteins, and qPCR to compare mitochondrial DNA levels and mRNA expression profiles. RNA-seq was performed in skeletal muscle. Ucp1-/- rats withstood 4°C for 14 days, but core temperature steadily declined. All rats lost body weight after 14 days at 4°C, but controls increased food intake more robustly than Ucp1-/- rats. Brown adipose tissue showed signs of decreased activity in Ucp1-/- rats, while mitochondrial lipid metabolism markers in white adipose tissue and skeletal muscle were increased. Ucp1-/- rats displayed more visible shivering and energy expenditure than controls at 4°C. Skeletal muscle transcriptomics showed more differences between genotypes at 23°C than at 4°C. Room temperature presented sufficient cold stress to rats lacking UCP1 to activate compensatory thermogenic mechanisms in skeletal muscle, which were only activated in control rats following exposure to 4°C. These results provide novel insight into thermogenic responses to UCP1 deficiency; and highlight Ucp1-/- rats as an attractive translational model for the study of thermogenesis.

SON-light activation of glucose regulation

Body temperature maintenance is an important regulator of glucose homeostasis. In this issue of Cell, Meng etal. discover a regulatory axis in which light activation of photoreceptive retinal ganglia stimulates the supraoptic nucleus (SON) to inhibit brown adipose tissue (BAT) thermogenesis and impair glucose homeostasis. This could explain the impact of constant light exposure on metabolism.

CUIDADO CIRÚRGIGO DE ENFERMAGEM EM SALAS DE CIRURGIA: UMA REVISÃO INTEGRATIVA

ABSTRACT Objective: to identify the state-of-the-art developed about surgical Nursing care in the operating room. Method: an integrative review with search and selection of primary studies conducted in April and May 2022 in four major data sources in the health field, namely: LILACS, SciELO, BDENF and PubMed, from 2018 to 2022. The sample consisted of 13 studies, 8 selected from a universe of 293 articles and 5 obtained through the manual search. Results: three categories were generated: Associating surgical care with care, people and material resources management for patient safety; Surgical care and ethical sensitivity in the search for patients' well-being; and Operating room nurses' manifestation and omission experiences and surgical care. Conclusions: surgical Nursing care in the operating room is varied and is manifested through meeting the administrative demands, ethical sensitivity, body temperature maintenance, preservation of individuality and meeting all the needs in the intraoperative period when patients are more vulnerable, including being duly informed as a way to provide safe surgical care. On the other hand, nurses acknowledge the need to change their world view and direct surgical care towards a more human, social and cultural perspective.

Recruitment of Muscle Genes as an Effect of Brown Adipose Tissue Ablation in Cold-Acclimated Brandt’s Voles (Lasiopodomys brandtii)

Skeletal muscle-based nonshivering thermogenesis (NST) plays an important role in the regulation and maintenance of body temperature in birds and large mammals, which do not contain brown adipose tissue (BAT). However, the relative contribution of muscle-based NST to thermoregulation is not clearly elucidated in wild small mammals, which have evolved an obligate thermogenic organ of BAT. In this study, we investigated whether muscle would become an important site of NST when BAT function is conditionally minimized in Brandt's voles (Lasiopodomys brandtii). We surgically removed interscapular BAT (iBAT, which constitutes 52%~56% of total BAT) and exposed the voles to prolonged cold (4 °C) for 28 days. The iBAT-ablated voles were able to maintain the same levels of NST and body temperature (~37.9 °C) during the entire period of cold acclimation as sham voles. The expression of uncoupling protein 1 (UCP1) and its transcriptional regulators at both protein and mRNA levels in the iBAT of cold-acclimated voles was higher than that in the warm group. However, no difference was observed in the protein or mRNA levels of these thermogenesis-related markers except for PGC-1α in other sites of BAT (including infrascapular region, neck, and axilla) between warm and cold groups either in sham or iBAT-ablated voles. The iBAT-ablated voles showed higher UCP1 expression in white adipose tissue (WAT) than sham voles during cold acclimation. The expression of sarcolipin (SLN) and sarcoplasmic endoplasmic reticulum Ca2+-dependent adenosine triphosphatase (SERCA) in skeletal muscles was higher in cold than in warm, but no alteration in phospholamban (PLB) and phosphorylated-PLB (P-PLB) was observed. Additionally, there was increased in iBAT-ablated voles compared to that in the sham group in cold. Moreover, these iBAT-ablated voles underwent extensive remodeling of mitochondria and genes of key components related with mitochondrial metabolism. These data collectively indicate that recruitment of skeletal muscle-based thermogenesis may compensate for BAT impairment and suggest a functional interaction between the two forms of thermogenic processes of iBAT and skeletal muscle in wild small mammals for coping cold stress.