Cold Exposure Research Articles

Hot and cold exposure triggers distinct transcriptional and behavioral responses in laboratory-inbred pond snails

Animals exhibit remarkable behavioral and molecular adaptations to cope with thermal stressors, which are crucial for survival in variable environments that are exacerbated by climate change. Aquatic poikilotherms like our model organism—the pond snail Lymnaea stagnalis—face significant challenges due to their dependence on external temperatures. Our study provides valuable insights into the different behavioral and molecular responses of lab-inbred snails to cold and heat shock stressors (i.e., 4 °C and 30 °C), particularly in the context of learning and memory formation. We found that while short-term (1 h) cold exposure transiently upregulated the expression levels of HSP70 and HSP40 in the snail’s central ring ganglia, prolonged cold exposure (24 h) resulted in a significant downregulation of LymMIPII and an upregulation of LymMIPR. These data suggest, albeit at the transcriptional level, the existence of a negative feedback loop necessary for sustaining cellular functions when metabolic demands might shift towards conserving energy during prolonged cold exposure. At the behavioral level, we found that, compared to heat shock, cold exposure did not result in a Garcia effect (i.e., a “special form” of conditioned taste aversion). The difference in memory outcomes was associated with changes in the expression levels of selected targets involved in neuronal plasticity and the stress response. While both cold and heat shock upregulated the HSP levels in the snail's central ring ganglia, cold exposure did not affect the expression levels of the neuroplasticity genes LymGRIN1 and LymCREB1, contrasting with heat shock’s neurogenic effects. Overall, this study provides insights into L. stagnalis's adaptive responses to thermal stressors, emphasizing different molecular strategies for coping with heat versus cold challenges in aquatic environments. These findings contribute to our understanding of thermal biology and stress physiology in aquatic organisms, underscoring the importance of molecular mechanisms in shaping species' resilience in dynamic environments.

Sex differences in physiological responses and thermal perception during repeated extremely cold exposure (−15 °C)

People working in cold regions often need to move frequently between indoor and outdoor environments. Due to sex differences in metabolic rates and thermal sensitivity, repeated exposure to large temperature differences may stress physiological and perceptual systems of males and females differently. This study aims to explore the physiological responses and thermal perception changes in males and females repeatedly exposed to −15 °C. The experiment involved 20 participants (gender balanced), who experienced two consecutive cycles of cold exposure. Each cycle included 30 min of cold exposure and 30 min of recovery. During the experiment, multiple physiological parameters as well as overall and local thermal perception were recorded. The experimental results indicate that repeated cold exposure can lead to thermal habituation in both males and females. Males exhibited higher skin temperatures in extremities such as the hands, fingers, face, and feet, while females reported lower thermal sensations in these areas during the recovery period. Furthermore, repeated cold exposure has a greater impact on the rate of recovery of extremity skin temperatures in females, requiring a longer recovery time compared to males. This article has reference value for considering sex differences in the design of temporary transition spaces in winter, which is beneficial to improving thermal comfort and energy efficiency.

Association of brown adipose tissue activity with circulating sex hormones and fibroblast growth factor 21 in the follicular and luteal phases in young women

BackgroundThermogenesis is influenced by fluctuations in sex hormones during the menstrual cycle in premenopausal women. The thermogenic activity and mass of brown adipose tissue (BAT) are regulated by endocrine factors, including sex hormones and fibroblast growth factor 21 (FGF21). However, the relationship between human BAT and these endocrine fluctuations within individuals remains to be elucidated. This study aimed to assess variations in BAT activity between the luteal and follicular phases and identify correlations with circulating levels of sex hormones and FGF21.MethodsHealthy young women were enrolled in an observational study. Measurement of BAT activity and blood analyses were performed in both the follicular and luteal phases. BAT activity was analyzed using thermography with 2-h cold exposure. Plasma 17β-estradiol, progesterone, and FGF21 levels were determined by enzyme-linked immunosorbent assay. A comparative analysis within individuals was conducted in 13 women to compare the follicular and luteal phases. Furthermore, sensitivity analysis was carried out in 21 women during the follicular phase only.ResultsPlasma 17β-estradiol and progesterone levels were significantly higher in the luteal phase, whereas plasma FGF21 level was significantly higher in the follicular phase. Comparison analysis found no significant differences in cold-induced BAT activity between the follicular and luteal phases in young women. Correlation analysis in both comparison and sensitivity analyses found that plasma 17β-estradiol and progesterone levels were not associated with BAT activity, whereas plasma FGF21 levels were significantly and positively correlated with BAT activity only in the follicular phase. In addition, plasma 17β-estradiol levels in the follicular phase were significantly and positively associated with plasma FGF21 levels in both the comparison and sensitivity analyses.ConclusionsThe thermogenic activity of BAT during cold exposure was comparable between the follicular and luteal phases in young women. Higher BAT activity was associated with elevated levels of plasma FGF21 only in the follicular phase, which is related to increased plasma 17β-estradiol levels.

Cardiovascular responses to heat and cold exposure are altered by preterm birth in guinea pigs.

Adversity early in life can modify the trajectory for disease risk extending decades beyond the event. Preterm birth produces persistent cardiovascular alterations that may appear maladaptive in adulthood. We have previously hypothesized that those born preterm may exhibit cardiovascular vulnerability in the climate change context. Further, this vulnerability may be present as early as childhood. We aimed to identify the early signs of cardiovascular dysfunction at childhood-equivalent age using our animal model of preterm birth. Using a whole-body thermal stress test, guinea pigs aged 35-d and 38-d (equivalent to 8-10-year-old children) and born at term or preterm gestations were exposed to progressive hyper- (TC = 41.5°C) and hypo-thermia (TC = 34°C; normothermia TC = 39°C). Comprehensive cardiovascular monitoring included ECG, blood pressure, microvascular perfusion, blood gas, and catecholamine profile, as well as skin and core body temperature. Preterm-born animals exhibited attenuated vascular responses to hyperthermic stress, and a significant elevation in systolic blood pressure in response to hypothermic stress. Such responses are similar to those observed in elderly populations and indicate the presence of cardiovascular dysfunction. This is the first study to demonstrate the impact of preterm birth on the cardiovascular response to both heat and cold stress. Further, this dysfunction has been observed at an earlier age than that achievable using traditional stress testing techniques. The present findings warrant further investigation.

Effective Prevention and Treatment of Acute Leukemias in Mice by Activation of Thermogenic Adipose Tissues.

Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) are common hematological malignancies in adults. Despite considerable research advances, the development of standard therapies, supportive care, and prognosis for the majority of AML and ALL patients remains poor and the development of new effective therapy is urgently needed. Here, it is reported that activation of thermogenic adipose tissues (TATs) by cold exposure or β3-adrenergic receptor agonists markedly alleviated the development and progression of AML and ALL in mouse leukemia models. TAT activation (TATA) monotherapy substantially reduces leukemic cells in bone marrow and peripheral blood, and suppresses leukemic cell invasion, including hepatomegaly and splenomegaly. Notably, TATA therapy prolongs the survivals of AML- and ALL-bearing mice. Surgical removal of thermogenic brown adipose tissue (BAT) or genetic deletion of uncoupling protein 1 (UCP1) largely abolishes the TATA-mediated anti-leukemia effects. Metabolomic pathway analysis demonstrates that glycolytic metabolism, which is essential for anabolic leukemic cell growth, is severely impaired in TATA-treated leukemic cells. Moreover, a combination of TATA therapy with chemotherapy produces enhanced anti-leukemic effects and reduces chemotoxicity. These data provide a new TATA-based therapeutic paradigm for the effective treatment of AML, ALL, and likely other types of hematological malignancies.

Structural basis of respiratory complex adaptation to cold temperatures.

In response to cold, mammals activate brown fat for respiratory-dependent thermogenesis reliant on the electron transport chain. Yet, the structural basis of respiratory complex adaptation upon cold exposure remains elusive. Herein, we combined thermoregulatory physiology and cryoelectron microscopy (cryo-EM) to study endogenous respiratory supercomplexes from mice exposed to different temperatures. A cold-induced conformation of CI:III2 (termed type 2) supercomplex was identified with a ∼25° rotation of CIII2 around its inter-dimer axis, shortening inter-complex Q exchange space, and exhibiting catalytic states that favor electron transfer. Large-scale supercomplex simulations in mitochondrial membranes reveal how lipid-protein arrangements stabilize type 2 complexes to enhance catalytic activity. Together, our cryo-EM studies, multiscale simulations, and biochemical analyses unveil the thermoregulatory mechanisms and dynamics of increased respiratory capacity in brown fat at the structural and energetic level.

Muti-omics revealed the mechanisms of MT-conferred tolerance of Elymus nutans Griseb. to low temperature at XiZang

BackgroundLow temperature seriously limited the development of grass and crops in plateau. Thus, it is urgent to develop an effective strategy for improving the plant cold tolerance and elucidate the underlying mechanisms.ResultsWe found that MT alleviated the effects of cold stress on suppressing ENG growth, then improved cold tolerance of ENG. Integration of transcriptome and metabolome profiles showed that both cold exposure (TW) and MT reprogrammed the transcription pattern of galactose and flavonoids biosynthesis, leading to changes in compositions of soluble sugar and flavonoids in ENG. Additionally, TW inhibited the photosynthesis, and destroyed the antioxidant system of ENG, leading to accumulation of oxidant radicals represented by MDA. By contrast, MT promoted activities of antioxidant enzymes and flavonoid accumulation in ENG under cold condition, then reduced the MDA content and maintained normal expression of photosynthesis-related genes in ENG even under TW. Importantly, MT mainly enhanced cold tolerance of ENG via activating zeatin synthesis to regulate flavonoid biosynthesis in vivo. Typically, WRKY11 was identified to regulate MT-associated zeatin synthesis in ENG via directly binding on zeatin3 promoter.ConclusionsMT could enhance ENG tolerance to cold stress via strengthening antioxidant system and especially zeatin synthesis to promote accumulation of flavonoids in ENG. Thus, our research gain insight into the global mechanisms of MT in promoting cold tolerance of ENG, then provided guidance for protecting plant from cold stress in plateau.

Keys to the switch of fat burning: stimuli that trigger the uncoupling protein 1 (UCP1) activation in adipose tissue.

As one of the main pathogenic factors of cardiovascular and cerebrovascular diseases, the incidence of metabolic diseases such as adiposity and metabolic dysfunction-associated steatotic liver disease (MASLD) is increasing annually. It is urgent and crucial to find more therapeutic targets to treat these diseases. Mainly expressed in brown adipocytes, mitochondrial uncoupling protein 1 (UCP1) is key to the thermogenesis of classical brown adipose tissue (BAT). Furthermore, white adipose tissue (WAT) is likely to express more UCP1 and subsequently acquire the ability to undergo thermogenesis under certain stimuli. Therefore, targeting and activating UCP1 to promote increased BAT thermogenesis and browning of WAT are helpful in treating metabolic diseases, such as adiposity and MASLD. In this case, the stimuli that activate UCP1 are emerging. Therefore, we summarize the thermogenic stimuli that have activated UCP1 in recent decades, among which cold exposure is one of the stimuli first discovered to activate BAT thermogenesis. As a convenient and efficient therapy with few side effects and good metabolic benefits, physical exercise can also activate the expression of UCP1 in adipose tissue. Notably, for the first time, we have summarized and demonstrated the stimuli of traditional Chinese medicines that can activate UCP1, such as acupuncture, Chinese herbal formulas, and Chinese medicinal herbs. Moreover, pharmacological agents, functional foods, food ingredients, and the gut microbiota are also commonly associated with regulating and activating UCP1. The identification and analysis of UCP1 stimuli can greatly facilitate our understanding of adipose tissue thermogenesis, including the browning of WAT. Thus, it is more conducive to further research and therapy for glucose and lipid metabolism disorders.

Effect of Cold Exposure on the Biofoam Produced from Different Types of Oyster Mushroom

Mycelium-based biofoam is a sustainable material derived from the growth of fungal mycelium on lignocellulosic agricultural waste substrate, as it has potential use in a variety of applications. The main objective of this research is to advance the sustainable alternatives for various application by investigating the mycelium growth of the biofoam produced from Pleurotus florida and Pleurotus sajor-caju on rice husk substrate, in improving the properties of the biofoam through innovative cold exposure. This study showed P. florida can produce mycelium biofoam at a faster rate, 7.022mm/day compared to P. sajor-caju 6.08mm/day). By cold exposure at 0°C and 10°C for 3 hours, every 2 days and 5 days, respectively until the mycelium are fully grown in the substrate, sample exposed to the latter condition for P. florida exhibits a faster growth rate at 7.3037 mm/day. However, cold exposure on biofoam produced from P sajor-caju had not improved the mycelium growth rate. Cold exposure samples at 0°C every 5 days and 10°C every 2 days have demonstrated capability in water (103.51%) and oil absorption (143.23%), proving their effectiveness in absorbing pollutants for the purpose of environmental remediation. The FTIR analysis confirmed the presence of hydrophilic and oleophilic characteristics in the biofoam, indicating its capability to absorb water and oil. By subjecting biofoam to cold exposure, its properties can be altered, broadening its potential applications.

Differential mitochondrial adaptation and FNDC5 production in brown and white adipose tissue in response to cold and obesity.

Fibronectin type III domain-containing protein 5 (FNDC5) modulates adipocyte metabolism by increasing white and brown adipose tissue (WAT and BAT) browning and activity, respectively. We investigated whether FNDC5 can regulate visceral WAT and BAT adaptive thermogenesis by improving mitochondrial homeostasis in response to cold and obesity. Adipose tissue expression of FNDC5 and factors involved in mitochondrial homeostasis were determined in patients with normal weight and obesity (n = 159) and in rats with diet-induced obesity after 1 week of cold exposure (n = 61). The effect of different FNDC5 concentrations on mitochondrial biogenesis, dynamics, and mitophagy was evaluated in vitro in human adipocytes. In human visceral adipocytes, FNDC5/irisin triggered mitochondrial biogenesis (TFAM) and fusion (MFN1, MFN2, and OPA1) while inhibiting peripheral fission (DNM1L and FIS1) and mitophagy (PINK1 and PRKN). Circulating and visceral WAT expression of FNDC5 wasdecreased in patients and experimental animals with obesity, whereas its receptor, integrin αV, was upregulated. Obesity increased mitochondrial fusion while decreasing mitophagy in visceral WAT from patients and rats. By contrast, in rat BAT, an upregulation of Fndc5 and genes involved in mitochondrial biogenesis and fission was observed. Cold exposure promoted mitochondrial biogenesis and healthy peripheral fission while repressing Fndc5 expression and mitophagy in BAT from rats. Depot differences in FNDC5 production and mitochondrial adaptations in response to obesity and cold might indicate a self-regulatory mechanism to control thermogenesis in response to energy needs.

Slit3 Fragments Orchestrate Neurovascular Expansion and Thermogenesis in Brown Adipose Tissue.

Brown adipose tissue (BAT) represents an evolutionary innovation enabling placental mammals to regulate body temperature through adaptive thermogenesis. Brown adipocytes are surrounded by a dense network of blood vessels and sympathetic nerves that support their development and thermogenic function. Cold exposure stimulates BAT thermogenesis through the coordinated induction of brown adipogenesis, angiogenesis, and sympathetic innervation. However, how these distinct processes are coordinated remains unclear. Here, we identify Slit guidance ligand 3 (Slit3) as a new niche factor that mediates the crosstalk among adipocyte progenitors, endothelial cells, and sympathetic nerves. We show that adipocyte progenitors secrete Slit3 which regulates both angiogenesis and sympathetic innervation in BAT and is essential for BAT thermogenesis in vivo. Proteolytic cleavage of Slit3 generates secreted Slit3-N and Slit3-C fragments, which activate distinct receptors to stimulate angiogenesis and sympathetic innervation, respectively. Moreover, we introduce bone morphogenetic protein-1 (Bmp1) as the first Slit protease identified in vertebrates. In summary, this study underscores the essential role of Slit3-mediated neurovascular network expansion in enabling cold-induced BAT adaptation. The co-regulation of neurovascular expansion by Slit3 fragments provides a bifurcated yet harmonized approach to ensure a synchronized response of BAT to environmental challenges. This study presents the first evidence that adipocyte progenitors regulate tissue innervation, revealing a previously unrecognized dimension of cellular interaction within adipose tissue.

Effects of intermittent exposure to hypobaric hypoxia and cold on skeletal muscle regeneration: Mitochondrial dynamics, protein oxidation and turnover

Muscle injuries and the subsequent regeneration events compromise muscle homeostasis at morphological, functional and molecular levels. Among the molecular alterations, those derived from the mitochondrial function are especially relevant. We analysed the mitochondrial dynamics, the redox balance, the protein oxidation and the main protein repairing mechanisms after 9 days of injury in the rat gastrocnemius muscle. During the recovery rats were exposed to intermittent cold exposure (ICE), intermittent hypobaric hypoxia (IHH), and both simultaneous combined stimuli. Non-injured contralateral legs were also analysed to evaluate the specific effects of the three environmental exposures. Our results showed that ICE enhanced mitochondrial adaptation by improving the electron transport chain efficiency during muscle recovery, decreased the expression of regulatory subunit of proteasome and accumulated oxidized proteins. Exposure to IHH did not show mitochondrial compensation or increased protein turnover mechanisms; however, no accumulation of oxidized proteins was observed. Both ICE and IHH, when applied separately, elicited an increased expression of eNOS, which could have played an important role in accelerating muscle recovery. The combined effect of ICE and IHH led to a complex response that could potentially impede optimal mitochondrial function and enhanced the accumulation of protein oxidation. These findings underscore the nuanced role of environmental stressors in the muscle healing process and their implications for optimizing recovery strategies.

The Skin's Sun Story: Risks and Precautions

Background: The skin, representing the largest organ in the human body, serves numerous funtions crucial for homeostasis, as well as acts as the primary physical barrier protecting the organism from external environmental factors such as microorganisms, mechanical damage, heat or cold exposure, toxins, as well as solar radiation, posing various risks to the skin, including sunburn, photoageing and skin malignancies. Objectives: This study aims to explore the effects of solar radiation on the skin and to discuss preventive measures against its negative influence on the skin. Methods: An exhaustive search of references related to sun exposure and skin published in PubMed was undertaken, using the search terms: "solar exposure and skin, ultraviolet radiation and skin, visible light and skin, sunscreen, photoprotection”. Conclusions: Solar radiation, particularly ultraviolet radiation (UVR), induces acute and chronic damage to the skin, leading to conditions such as sunburn, photoaging, and skin malignancies. However, adequate exposure to sunlight is crucial for the synthesis of vitamin D3, which plays essential roles in calcium homeostasis, immune function, and potentially other physiological processes. Strategies such as proper sunscreen use and other photoprotection methods can mitigate the adverse effects of solar radiation while allowing for sufficient vitamin D synthesis.

Application of hot water and cold air to reduce bacterial contamination on broiler carcasses.

Two physical treatments (heat via water bath and cold air) with various temperatures (20/70/75/80°C and - 80/-90°C) and exposure times (20, 30, 40 s) were carried out to identify a decontaminating effect on zoonotic pathogens on broiler carcasses. Subsequently, carcasses were analyzed for thermotolerant Campylobacter (C.), Salmonella, Escherichia (E.). coli and total colony count (TCC). Moreover, for the hot water treatment, qPCR with viable/dead differentiation (v-qPCR) was applied to detect viable but non-culturable cells (VBNC) of Campylobacter, referred to as intact but putatively infectious units (IPIU). Hot water immersion was tested on carcasses inoculated with C. jejuni and Salmonella, while cold air treatment was evaluated for naturally contaminated carcasses of broiler flocks colonized with Campylobacter. For hot water treatment, the statistically significant reducing effect was about 1 log10 CFU/ml for both Salmonella and Campylobacter for 70-80°C and 20/30 s treatments. The effect of heat treatment for Campylobacter was smaller when samples were analyzed with v-qPCR with reductions of 0.5-0.8 log10 IPIU/ml in mean. Cold air treatments at -90°C were effective in reducing the mean contamination level of Campylobacter by 0.4-0.5 log10 CFU/ml at all exposure times (p < 0.05). Hot water treatments showed a decreasing trend on TCC by 0.6-0.9 log10 CFU/ml (p < 0.05). TCC counts were not significantly affected by cold air treatment. For E. coli no statistically significant reductions were observed by hot water treatment. The cold air treatment at -90°C for 20 and 40 s led to a reduction of E. coli by 0.4 and 0.8 log10 CFU/ml (p < 0.05), respectively. Treatment of carcasses with higher bacterial levels tended to show higher reduction. The research demonstrated that the efficacy of physical treatments for decontamination of broiler carcasses was more pronounced for hot water immersion than for cold air exposure. In conclusion, the results shed light on the potential application of these physical treatments in practice to reduce the quantitative load of contaminating pathogens to enhance food safety in the broiler meat production.

Modelling time-temperature-dependent mortality of pest flies in cold storage to support the management of trade-related biosecurity risks

AbstractCold treatment with rigorous regulatory oversight is often mandated to manage horticultural trade-related biosecurity threats, such as invasive, cold-sensitive fruit flies (Diptera: Tephritidae). Cold treatment schedules, developed through rigorous laboratory experiments, require a set temperature and duration to ensure at least a probit 8.7 (99.99%) mortality rate, regardless of infestation likelihood. This threshold is costly to demonstrate for each pest and commodity combination and the resultant treatment may be harmful to fruit quality. Moreover, these stringent schedules do not account for cold-induced mortality already occurring in commercial supply chains. We developed a predictive temperature-dependent mortality function using 28 published cold treatment studies of pest fly species to support more flexible and proportionate use of cold treatment. The daily mortality rate was unaffected by the duration of cold exposure (0–20 days). The mortality rate varied primarily by pest species (10 species) and developmental stage (eggs and larval stages), and to a lesser extent by temperature (0–7 °C) and host (13 fruit types). Our model mostly predicted fewer days to meet probit 9.0 mortality compared to empirical results from large-scale studies, suggesting these studies can be overly conservative. By leveraging previous empirical studies, our model enables estimation of temperature-dependent daily mortality for unstudied pest developmental stage host–temperature combinations, which can then be empirically validated through targeted studies. It is hoped these results will shift cold treatment usage from highly regulated, fixed temperature treatments with a target mortality rate requirement to a more flexible approach that accounts for existing commercial supply chain practices and infestation likelihood in produce.

Cold exposure accelerates lysine catabolism to promote cold acclimation via remodeling hepatic histone crotonylation

BackgroundCold environments pose serious threats on human health, with increased risk for myocardial infarction, stroke, frostbite, and hypothermia. Acquired cold acclimation is required to minimize cold-induced injures and to improve metabolic health. However, the underlying mechanisms remain to be fully elucidated. ObjectiveWe aimed to identify critical amino acids involved in cold acclimation and unmask the regulatory mechanisms. MethodsA total of twenty male participants were recruited and followed up after 3 months’ natural cold exposure. Cold-induced vasodilation (CIVD) tests and clinical biochemical analysis were performed at baseline and after 3-months cold exposure, whilst blood samples were collected, and plasma amino acids were analyzed by targeted metabolomics. To further confirm the effect of lysine on cold tolerance and explain the latent mechanism, mice were challenged with chronic cold exposure for 7 days with lysine supplement, then core and local surface temperature as well as thermogenesis activity were detected. ResultsContinuous cold exposure shortened the CIVD onset time and increased the average finger temperature. Levels of the plasma lysine and glycine were decreased in both humans and mice. Venn analysis from three datasets revealed that lysine was the only significantly changed plasma amino acid, which strongly correlated with the altered CIVD. Moreover, mice sustained a relatively higher core temperature and surface temperature in the back, tail and paws upon lysine supplementation. Furthermore, lysine supplementation increased the level of histone H3K18cr and promoted the gene and protein expression of Cpt1a, Cpt2 and Cyp27a1 in liver. ConclusionOur work identified lysine as a critical amino acid for the remodeling of hepatic histone crotonylation that facilitates cold acclimation.

Reversing Pdgfrβ signaling restores metabolically active beige adipocytes by alleviating ILC2 suppression in aged and obese mice

ObjectivePlatelet Derived Growth Factor Receptor Beta (Pdgfrβ) suppresses the formation of cold temperature-induced beige adipocytes in aged mammals. We aimed to determine if deleting Pdgfrβ in aged mice could rejuvenate metabolically active beige adipocytes by activating group 2 innate lymphoid cells (ILC2), and whether this effect could counteract diet-induced obesity-associated beige fat decline. MethodsWe employed Pdgfrβ gain-of-function and loss-of-function mouse models targeting beige adipocyte progenitor cells (APCs). Our approach included cold exposure, metabolic cage analysis, and age and diet-induced obesity models to examine beige fat development and metabolic function under varied Pdgfrβ activity. ResultsAcute cold exposure alone enhanced metabolic benefits in aged mice, irrespective of beige fat generation. However, Pdgfrβ deletion in aged mice reestablished the formation of metabolically functional beige adipocytes, enhancing metabolism. Conversely, constitutive Pdgfrβ activation in young mice stymied beige fat development. Mechanistically, Pdgfrβ deletion upregulated IL-33, promoting ILC2 recruitment and activation, whereas Pdgfrβ activation reduced IL-33 levels and suppressed ILC2 activity. Notably, diet-induced obesity markedly increased Pdgfrβ expression and Stat1 signaling, which inhibited IL-33 induction and ILC2 activation. Genetic deletion of Pdgfrβ restored beige fat formation in obese mice, improving whole-body metabolism. ConclusionsThis study reveals that cold temperature exposure alone can trigger metabolic activation in aged mammals. However, reversing Pdgfrβ signaling in aged and obese mice not only restores beige fat formation but also renews metabolic function and enhances the immunological environment of white adipose tissue (WAT). These findings highlight Pdgfrβ as a crucial target for therapeutic strategies aimed at combating age- and obesity-related metabolic decline.

Cold induces brain region-selective cell activity-dependent lipid metabolism.

It has been well documented that cold is an enhancer of lipid metabolism in peripheral tissues, yet its effect on central nervous system lipid dynamics is underexplored. It is well recognized that cold acclimations enhance adipocyte functions, including white adipose tissue (WAT) lipid lipolysis and beiging, and brown adipose tissue (BAT) thermogenesis in mammals. However, it remains unclear whether and how lipid metabolism in the brain is also under the control of cold acclimations. Here, we show that cold exposure predominantly increases the expressions of the lipid lipolysis genes and proteins within the paraventricular nucleus of the hypothalamus (PVH). Mechanistically, we find that cold activates cells within the PVH and pharmacological inactivation of cells blunts cold-induced effects on lipid peroxidation, accumulation of lipid droplets (LDs), and lipolysis in the PVH. Together, these findings suggest that PVH lipid metabolism is cold sensitive and integral to cold-induced broader regulatory responses.

Human body temperature and cardiovascular response to changes in ambient temperature and body posture

Health problems due to heat or cold exposure is closely related not only to body temperature (BT) but also to blood flow rate (BFR) and blood pressure (BP). Therefore, it is necessary to understand the physiological mechanisms of the human body, such as how these physiological quantities change and how they affect each other. In this study, to clarify the physiological mechanisms of the human body, we measured the whole-body distribution of BT and BFR, as well as BP, heart rate, and metabolic rate under changes in ambient temperature and body posture. A total of 19 subjects were tested in three cases, including the temperature up-step and down-step cases, where the ambient temperature changed from 28 °C to 38 °C or 18 °C in the supine position, and the posture change case, where the posture changed alternately between the supine and standing positions at an ambient temperature of 28 °C. The results showed that the core temperature was efficiently maintained due to BFR regulation, especially in the extremities, in response to changes in ambient temperature. Additionally, changes in cerebral BFR in response to changes in posture were suppressed due to regulation of BFR, especially in the lower limbs, and heart rate. Furthermore, in the extremities, the BFR not only in the skin but also in the subcutaneous tissue and muscle was estimated to increase in hot environments and decrease in cold environments.

Unravelling the interplay between Harmattan wind and baroreflex functions: implications on environmental health and cardiovascular pathophysiology

Harmattan is a season characterized by dust, cold, and sub-humid trade winds in Sub-Saharan countries. It’s similar to meteorological phenomena like Asian dust storms, Santa Ana winds, Australian bushfires, and Saharan dust in the Caribbean. It causes profound changes in the cardiorespiratory system in apparently healthy individuals and increases the risk of hospitalization in susceptible individuals. Exposure to these extreme conditions has been associated with alterations in autonomic function and baroreceptor sensitivity thus resulting in dysregulation of blood pressure control mechanisms. Baroreceptors are critical regulators of hemodynamics and cardiovascular function. They play a vital role in the short-term responses to blood pressure perturbation and are essential for acute restoration of blood pressure following cold exposure. Harmattan wind contains a barrage of chemicals, dust, and particulate matters depending on industrialization, natural and human activities. Particulate matter from Harmattan dust can trigger systemic inflammation and oxidative stress, exacerbating endothelial dysfunction and impairing vascular reactivity thus contributing to the pathogenesis of alterations in baroreceptor insensitivity, and cardiovascular diseases, including hypertension and atherosclerosis. Furthermore, fine particulate matter from dust may penetrate deep into the respiratory tract, activating pulmonary sensory receptors and eliciting reflex responses that influence autonomic tone. The presence of rich acrolein smokes and non-essential heavy metals such as cadmium, lead, and mercury in Harmattan wind also reduces baroreflex sensitivity, culminating in a sustained increase in diastolic and systolic blood pressure. This integrated review aims to provide valuable insights into how changes in each of these environmental constituents alter vital pathophysiologic and immunologic mechanisms of the body leading to baroreceptor instability and ultimately hemodynamic imbalance using available primary studies. Understanding this intricate interplay is crucial for implementing targeted interventions and informed public health strategies to mitigate the adverse effects of extreme environmental exposure and ultimately reduce poor health outcomes in the affected regions.