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Intermittent cold exposure (ICE) has garnered increased attention in popular culture, largely for its proposed effects on mood and immune function, but there are also suggestions that the energy-wasting mechanisms associated with thermogenesis may decrease body weight and fat mass. Considering the continued and worsening prevalence of obesity and type II diabetes, any protocol that can reduce body weight and/or improve metabolic health would be a substantial boon. Here, we present a narrative review exploring the research related to ICE and adipose tissue. Any publicly available original research examining the effects of repeated bouts of ICE on adipose-related outcomes was included. While ICE does not consistently lower body weight or fat mass, there does seem to be evidence for ICE as a positive modulator of the metabolic consequences of obesity, such as glucose tolerance and insulin signaling. Further, ICE consistently increases the activity of brown adipose tissue (BAT) and transitions white adipose tissue to a phenotype more in line with BAT. Lastly, the combined effects of ICE and exercise do not seem to provide any additional benefit, at least when exercising during ICE bouts. The majority of the current literature on ICE is based on rodent models where animals are housed in cold rooms, which does not reflect protocols likely to be implemented in humans such as cold water immersion. Future research could specifically characterize ICE via cold water immersion in combination with controlled calorie intake to clearly determine the effects of ICE as it would be implemented in humans looking to lower their body weight via reductions in fat mass.

Cold tolerance and potential distribution of Myllocerus undecimpustulatus undatus Marshall, a polyphagous pest in the United States, were investigated. Adult survivorship after 2 days at 0 °C and − 5 °C averaged 60% and 18%, respectively. Four days of exposure resulted in survivorship of 11% at 0 °C and 4% at − 5 °C, respectively. Summer-collected weevils at − 5 °C through repeated cold exposure of 2 h survived 3 times longer than those subjected to sustained cold period of 10 h. Leaf consumption did not differ among summer-collected weevils at constant 20 °C and repeated cold exposure treatments; weevils under sustained cold exposure consumed less than weevils in repeated cold exposure treatments. Leaf area consumed after cold exposure was 2–4 times greater in winter-collected weevils compared to summer-collected weevils. Leaf consumption by winter-collected weevils decreased as the number of repeated cold exposure periods increased. Locality data from collections in Florida during 2000–2012 were used to produce a correlative model complemented by a mechanistic model from the cold tolerance data to project the potential distribution of M. undecimpustulatus undatus in North America. The models support the hypothesis that M. undecimpustulatus undatus could spread to areas of the southeastern and western United States. The predicted northern distribution followed an isothermal line about 33° North. The niche model defined an area along the western Gulf Coast as unsuitable for the weevil, possibly because the area receives greater annual rainfall than other areas of the southeastern United States and has aquic or udic soil unlike the well-drained sandy soil of peninsular Florida.

Chronic or acute ambient temperature change alter the gut microbiota and the metabolites, regulating metabolic functions. Short-chain fatty acids (SCFAs) produced by gut bacteria reduce the risk of disease. Feeding patterns and gut microbiota that are involved in SCFAs production are controlled by the circadian clock. Hence, the effect of environmental temperature change on SCFAs production is expected depending on the exposure timing. In addition, there is limited research on effects of habitual cold exposure on the gut microbiota and SCFAs production compared to chronic or acute exposure. Therefore, the aim was to examine the effect of cold or heat exposure timing on SCFAs production. After exposing mice to 7 or 37 °C for 3 h a day at each point for 10 days, samples were collected, and cecal pH, SCFA concentration, and BAT weight was measured. As a result, cold exposure at ZT18 increased cecal pH and decreased SCFAs. Intestinal peristalsis was suppressed due to the cold exposure at ZT18. The results reveal differing effects of intermittent cold exposure on the gut environment depending on exposure timing. In particular, ZT18 (active phase) is the timing to be the most detrimental to the gut environment of mice.

Cold stress influences intestinal processes, causing physiological and immunological responses in animals. Intestinal microbiota participates in maintaining the stability of the intestinal environment. However, phenotypic characteristics and the effects of porcine microbiota changes under cold conditions remain poorly understood. Here, the fecal microbiota of cold tolerant breed (Mashen) and cold sensitive breed (Duroc-Landrace-Yorkshire) was transferred to germ-free mice, respectively. After a cold exposure (4°C) for 21 days, intestinal function and microbe changes of mice were explored. The results showed that Mashen pigs microbiota transplantation made the body temperature of the mice stable, in which the fat weight and expression of uncoupling protein 1 ( UCP 1), carnitine palmitoyltransferase 1B ( Cpt 1b), and Peroxisome proliferator-activated receptor-gamma coactivator ( PGC- 1α) were significantly higher ( P < 0.05) than those of the control group. The results of intestinal structure and expression of serum inflammatory factors showed that fecal microbiota transplantation (FMT) mice have more intact intestinal structure and high expression of proinflammatory factor such as interleukin-4 (IL-4). The study of mice fecal microbiome characterized via 16S rRNA sequencing found that pig microbiota transplantation changed the abundance of Firmicutes. In addition, it identified discriminative features of Firmicutes in the microbiota between two breeds of pig, in which Clostridiaceae were enriched in the microbiota community of Mashen pig and Coriobacteriales were significantly ( P < 0.05) enriched in the Duroc-Landrace-Yorkshire pig microbiota transplantation group based on linear discriminant analysis effect size (LEfSe) analysis. Finally, we found that the content of propionic acid and butyric acid in rectal contents significantly changed and the abundances of Clostridium and Lachnospira showed significant correlations with changes in short-chain fatty acids. The results suggest that pig fecal microbiota transplantation can alleviate the changes in physiological and biochemical indicators in mice caused by cold exposure. Mice have gut microbes altered and improved gut barrier function via fecal microbiota transplantation in pigs.

We use a suite of decadal-length regional climate simulations to quantify potential changes in population-weighted heat and cold exposure in 47 US metropolitan regions during the 21st century. Our results show that population-weighted exposure to locally defined extreme heat (i.e., “population heat exposure”) would increase by a factor of 12.7–29.5 under a high-intensity greenhouse gas (GHG) emissions and urban development pathway. Additionally, end-of-century population cold exposure is projected to rise by a factor of 1.3–2.2, relative to start-of-century population cold exposure. We identify specific metropolitan regions in which population heat exposure would increase most markedly and characterize the relative significance of various drivers responsible for this increase. The largest absolute changes in population heat exposure during the 21st century are projected to occur in major US metropolitan regions like New York City (NY), Los Angeles (CA), Atlanta (GA), and Washington DC. The largest relative changes in population heat exposure (i.e., changes relative to start-of-century) are projected to occur in rapidly growing cities across the US Sunbelt, for example Orlando (FL), Austin (TX), Miami (FL), and Atlanta. The surge in population heat exposure across the Sunbelt is driven by concurrent GHG-induced warming and population growth which, in tandem, could strongly compound population heat exposure. Our simulations provide initial guidance to inform the prioritization of urban climate adaptation measures and policy.

Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases.Estrogen might participate in neuroprotection after cold exposure,but its precise mechanism remains unclear.In this study,mice were exposed to 10°C for 7 days and 0–4°C for 30 days to induce a model of chronic cold exposure.Results showed that oxidative stress-related c-fos and cyclooxygenase 2 expressions,MAP1LC3-labeled autophagic cells,Iba1-labeled activated microglia,and interleukin-1β-positive pyramidal cells were increased in the hippocampal CA1 area.Chronic cold exposure markedly elevated the levels of estrogen in the blood and the estrogen receptor,G protein-coupled receptor 30.These results indicate that neuroimmunoreactivity is involved in chronic cold exposure-induced pathological alterations,including oxidative stress,neuronal autophagy,and neuroimmunoreactivity.Moreover,estrogen exerts a neuroprotective effect on cold exposure.

Background In mammals, cold exposure induces browning of white adipose tissue (WAT) and alters WAT gene expression and lipid metabolism to boost adaptive thermogenesis and maintain body temperature. Understanding the lipidomic and transcriptomic profiles of WAT upon cold exposure provides insights into the adaptive changes associated with this process. Results Here, we applied mass spectrometry and RNA sequencing (RNA-seq) to provide a comprehensive resource for describing the lipidomic or transcriptome profiles in cold-induced inguinal WAT (iWAT). We showed that short-term (3-day) cold exposure induces browning of iWAT, increases energy expenditure, and results in loss of body weight and fat mass. Lipidomic analysis shows that short-term cold exposure leads to dramatic changes of the overall composition of lipid classes WAT. Notably, cold exposure induces significant changes in the acyl-chain composition of triacylglycerols (TAGs), as well as the levels of glycerophospholipids and sphingolipids in iWAT. RNA-seq and qPCR analysis suggests that short-term cold exposure alters the expression of genes and pathways involved in fatty acid elongation, and the synthesis of TAGs, sphingolipids, and glycerophospholipids. Furthermore, the cold-induced lipid dynamics and gene expression pathways in iWAT are contrary to those previously observed in metabolic syndrome, neurodegenerative disorders, and aging, suggesting beneficial effects of cold-induced WAT browning on health and lifespan. Conclusion We described the significant alterations in the composition of glyphospholipids, glycerolipids, and sphingolipids and expression of genes involved in thermogenesis, fatty acid elongation, and fatty acid metabolism during the response of iWAT to short-term cold exposure. We also found that some changes in the levels of specific lipid species happening after cold treatment of iWAT are negatively correlated to metabolic diseases, including obesity and T2D.

Our study aims at identifying and quantifying the relationship between the cold and heat exposure and the risk of cardiovascular mortality through a systematic review and meta-analysis. A systematic review and meta-analysis were conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. Peer-reviewed studies about the temperature and cardiovascular mortality were retrieved in the MEDLINE, Web of Science, and Scopus databases from January 2000 up to the end of 2015. The pooled effect sizes of short-term effect were calculated for the heat exposure and cold exposure separately. Also, we assessed the dose-response relationship of temperature-cardiovascular mortality by a change in units of latitudes, longitude, lag days and annual mean temperature by meta-regression. After screening the titles, abstracts and full texts, a total of 26 articles were included in the meta-analysis. The risk of cardiovascular mortality increased by 5% (RR, 1.055; 95% CI [1.050-1.060]) for the cold exposure and 1.3% (RR, 1.013; 95% CI [1.011-1.015]) for the heat exposure. The short-term effects of cold and heat exposure on the risk of cardiovascular mortality in males were 3.8% (RR, 1.038; 95% CI [1.034-1.043]) and 1.1%( RR, 1.011; 95% CI [1.009-1.013]) respectively. Moreover, the effects of cold and heat exposure on risk of cardiovascular mortality in females were 4.1% (RR, 1.041; 95% CI [1.037-1.045]) and 1.4% (RR, 1.014; 95% CI [1.011-1.017]) respectively. In the elderly, it was at an 8.1% increase and a 6% increase in the heat and cold exposure, respectively. The greatest risk of cardiovascular mortality in cold temperature was in the 14 lag days (RR, 1.09; 95% CI [1.07-1.010]) and in hot temperatures in the seven lag days (RR, 1.14; 95% CI [1.09-1.17]). The significant dose-response relationship of latitude and longitude in cold exposure with cardiovascular mortality was found. The results showed that the risk of cardiovascular mortality increased with each degree increased significantly in latitude and longitude in cold exposure (0.2%, 95% CI [0.006-0.035]) and (0.07%, 95% CI [0.0003-0.014]) respectively. The risk of cardiovascular mortality increased with each degree increase in latitude in heat exposure (0.07%, 95% CI [0.0008-0.124]). Our findings indicate that the increase and decrease in ambient temperature had a relationship with the cardiovascular mortality. To prevent the temperature- related mortality, persons with cardiovascular disease and the elderly should be targeted. The review has been registered with PROSPERO (registration number CRD42016037673).

Objective The aim of the present study is to compare cold adaptation mechanisms between cold-tolerant Hezuo and cold-sensitive Bama pigs. Methods A total of 40 healthy pigs (75 days old), including 20 Hezuo pigs and 20 Bama pigs, were used in this study. A 2×2 factorial design was employed, with factors including breed (Hezuo vs. Bama) and ambient temperature (23±2°C vs. −15±2°C). After 7 days of acclimation, pigs in the cold groups were exposed to low temperature and slaughtered on days 0, 1, 5, and 10 (n = 5 per group per time point). All pigs had ad libitum access to feed and water. Lung histology, wet/dry ratio, oxidative and inflammatory biomarkers, apoptosis, and transcriptomics were analyzed. Results The results showed that Hezuo pigs displayed less severe alveolar septal thickening, inflammatory infiltration, and fine bronchial fold extension during cold exposure than Bama pigs. The W/D ratio dramatically decreased in Hezuo pigs while rising in Bama pigs. Hezuo pigs exhibited significantly higher aquaporin-1 (AQP-1) and aquaporin-5 (AQP-5) expressions than Bama pigs during the middle and late phases. Bama pigs displayed increased reactive oxygen species, malondialdehyde, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and decreased glutathione (GSH) levels. Hezuo pigs maintained stable GSH levels and no significant changes in late-phase inflammatory markers. Bama pigs had a greater apoptosis density and more TUNEL-positive cells than Hezuo pigs, which was related to the down-regulation of B-cell lymphoma 2 (Bcl-2) and the up-regulation of Bcl2-associated X protein (Bax) and Caspase-3. Transcriptomic analysis revealed that in Bama pigs, distinctive genes such as mucin 5B (MUC5B), matrix metallopeptidase 9 (MMP9), alveolar macrophage chemotactic factor-II (AMCF-II), interleukin 22 receptor subunit alpha 1 (IL22RA1), C-C motif chemokine ligand 16 (CCL16), SRY-box transcription factor 9 (SOX9), keratin 5 (KRT5) contribute to mucus hypersecretion, extracellular matrix degradation, and sustained inflammatory chemotaxis, worsening tissue damage. In contrast, Hezuo pigs possess unique genes such as aldehyde dehydrogenase 1 family member A2 (ALDH1A2), acyl-CoA synthetase long chain family member 6 (ACSL6), ACSM5, aldo-keto reductase family 1 member C1 (AKR1C1), nuclear receptor subfamily 4 group A member 3/2 (NR4A3/2), G protein subunit gamma 4 (GNG4), glycogen synthase 2 (GYS2), which enhance lipid metabolism, facilitate aldehyde detoxification, and mitigate oxidative stress, thereby orchestrating a cellular protection. Conclusion Hezuo pigs exhibit protective molecular mechanisms, suggesting potential targets for cold-resistance breeding.

Children, and particularly infants, have physiological, anatomic, and social factors that increase vulnerability to temperature extremes. We performed a systematic review to explore the association between acute adverse infant outcomes (children 0–1 years) and exposure to high and low ambient temperatures. MEDLINE (Pubmed), Embase, CINAHL Plus, and Global Health were searched alongside the reference lists of key papers. We included published journal papers in English that assessed adverse infant outcomes related to short-term weather-related temperature exposure. Twenty-six studies met our inclusion criteria. Outcomes assessed included: infant mortality (n = 9), sudden infant death syndrome (n = 5), hospital visits or admissions (n = 5), infectious disease outcomes (n = 5), and neonatal conditions such as jaundice (n = 2). Higher temperatures were associated with increased risk of acute infant mortality, hospital admissions, and hand, foot, and mouth disease. Several studies identified low temperature impacts on infant mortality and episodes of respiratory disease. Findings on temperature risks for sudden infant death syndrome were inconsistent. Only five studies were conducted in low- or middle-income countries, and evidence on subpopulations and temperature-sensitive infectious diseases was limited. Public health measures are required to reduce the impacts of heat and cold on infant health.