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Most mammalian cells have molecular circadian clocks that generate widespread rhythms in transcript and protein abundance. While circadian clocks are robust to fluctuations in the cellular environment, little is known about the mechanisms by which the circadian period compensates for fluctuating metabolic states. Here, we exploit the heterogeneity of single cells both in circadian period and a metabolic parameter--protein stability--to study their interdependence without the need for genetic manipulation. We generated cells expressing key circadian proteins (CRYPTOCHROME1/2 (CRY1/2) and PERIOD1/2 (PER1/2)) as endogenous fusions with fluorescent proteins and simultaneously monitored circadian rhythms and degradation in thousands of single cells. We found that the circadian period compensates for fluctuations in the turnover rates of circadian repressor proteins and uncovered possible mechanisms using a mathematical model. In addition, the stabilities of the repressor proteins are circadian phase dependent and correlate with the circadian period in a phase-dependent manner, in contrast to the prevailing model. [ABSTRACT FROM AUTHOR]

To determine whether mismatched energy intake and expenditure across the day and associated sex differences may be related with metabolic compensation and/or negative health outcomes, we assessed total-day and hourly energy balance (TDEB and EB), total-day and hourly energy intake (TDEI and EI), total-day and hourly energy expenditure (TDEE and EE) and within-day energy balance (WDEB) in elite male and female swimmers (n = 25; 18–22 years). Total triiodothyronine (TT3), resting metabolic rate (RMR), and the ratio of actual-to-predicted RMR were determined. Males exhibited higher TDEB (+758 ± 702 kcal vs +52 ± 505 kcal, t-test; p = 0.007) than females. Males exhibited a more positive hourly EB, driven by greater hourly EI at 11:00, 13:00, 16:00, and 19:00 h (ANOVA, p < 0.05), while EE did not differ. TT3 was negatively correlated with consecutive hours of negative EB (R = −0.604, p = 0.049) and positively correlated to hours in EB (R = 0.740, p = 0.009) in those exhibiting metabolic suppression (n = 12). In individuals in TDEB (n = 21), "backloaders" (consumption of ≥50% daily kcals at or after 1700 h) had lower TT3 (79.3 ng/dL vs 92.9 ng/dL, p = 0.009) than "nonbackloaders" (n = 12). WDEB analyses indicate a greater risk of energy deficiency in females and may capture indices of metabolic compensation not evident with EB analyses alone. [ABSTRACT FROM AUTHOR]

The acquisition of fertilizing ability by mammalian spermatozoa, known as “capacitation,” includes processes that depend on particular metabolic pathways. This has led to the hypothesis that ATP demands might differ between capacitated and non-capacitated cells. Mouse sperm can produce ATP via OXPHOS and aerobic glycolysis, an advantageous characteristic considering that these cells have to function in the complex and variable environment of the female reproductive tract. Nonetheless, despite evidence showing that both metabolic pathways play a role in events associated with mouse sperm capacitation, there is contradictory evidence regarding changes promoted by capacitation in this species. In addition, the vast majority of studies regarding murine sperm metabolism use Mus musculus laboratory strains as model, thus neglecting the wide diversity of sperm traits of other species of Mus. Focus on closely related species with distinct evolutionary histories, which may be the result of different selective pressures, could shed light on diversity of metabolic processes. Here, we analyzed variations in sperm bioenergetics associated with capacitation in spermatozoa of the steppe mouse, Mus spicilegus, a species with high sperm performance. Furthermore, we compared sperm metabolic traits of this species with similar traits previously characterized in M. musculus. We found that the metabolism of M. spicilegus sperm responded to capacitation in a manner similar to that of M. musculus sperm. However, M. spicilegus sperm showed distinct metabolic features, including the ability to perform cross-pathway metabolic compensation in response to either respiratory or glycolytic inhibition, thus revealing a delicate fine-tuning of its metabolic capacities. [ABSTRACT FROM AUTHOR]

Rare subpopulations of cancer stem cells (CSCs) have the ability to self-renew and are the primary driving force behind cancer metastatic dissemination and the preeminent hurdle to cancer treatment. As opposed to differentiated, non-malignant tumor offspring, CSCs have sophisticated metabolic patterns that, depending on the kind of cancer, rely mostly on the oxidation of major fuel substrates such as glucose, glutamine, and fatty acids for survival. Glutaminolysis is a series of metabolic reactions that convert glutamine to glutamate and, eventually, α-ketoglutarate, an intermediate in the tricarboxylic acid (TCA) cycle that provides biosynthetic building blocks. These building blocks are mostly utilized in the synthesis of macromolecules and antioxidants for redox homeostasis. A recent study revealed the cellular and molecular interconnections between glutamine and cancer stemness in the cell. Researchers have increasingly focused on glutamine catabolism in their attempt to discover an effective therapy for cancer stem cells. Targeting catalytic enzymes in glutaminolysis, such as glutaminase (GLS), is achievable with small molecule inhibitors, some of which are in early-phase clinical trials and have promising safety profiles. This review summarizes the current findings in glutaminolysis of CSCs and focuses on novel cancer therapies that target glutaminolysis in CSCs. [ABSTRACT FROM AUTHOR]

Steele, Andrew R., Philip N. Ainslie, Rachel Stone, Kaitlyn Tymko, Courtney Tymko, Connor A. Howe, David MacLeod, James D. Anholm, Christopher Gasho, and Michael M. Tymko. Global REACH 2018: characterizing acid–base balance over 21 days at 4,300 m in lowlanders. High Alt Med Biol. 23:185–191, 2022. Introduction: High altitude exposure results in hyperventilatory-induced respiratory alkalosis, followed by metabolic compensation to return arterial blood pH (pHa) toward sea level values. However, previous work has limited sample sizes, short-term exposure, and pharmacological confounders (e.g., acetazolamide). The purpose of this investigation was to characterize acid–base balance after rapid ascent to high altitude (i.e., 4,300 m) in lowlanders. We hypothesized that despite rapid bicarbonate ([HCO3−]) excretion during early acclimatization, partial respiratory alkalosis would still be apparent as reflected in elevations in pHa compared with sea level after 21 days of acclimatization to 4,300 m. Methods: In 16 (3 female) healthy volunteers not taking any medications, radial artery blood samples were collected and analyzed at sea level (150 m; Lima, Peru), and on days 1, 3, 7, 14, and 21 after rapid automobile (∼8 hours) ascent to high altitude (4,300 m; Cerro de Pasco, Peru). Results and Discussion: Although reductions in [HCO3−] occurred by day 3 (p < 0.01), they remained stable thereafter and were insufficient to fully normalize pHa back to sea level values over the subsequent 21 days (p < 0.01). These data indicate that only partial compensation for respiratory alkalosis persists throughout 21 days at 4,300 m. [ABSTRACT FROM AUTHOR]

The relationship between daily energy expenditure (DEE) and resting metabolic rate (RMR) provides insight into how organisms allocate energy to maintenance versus energetically expensive activities such as locomotor activity.Three models have been devised to describe energy management: the allocation, independent and performance models, which, respectively, predict a DEE–RMR slope of b < 1, b = 1 and b > 1.Here, we took paired repeated metabolic and behavioural measurements in 51 female white‐footed mice to (a) evaluate which energy management models apply at the among‐ and within‐individual levels and to (b) quantify the relationship between metabolic traits and two energetically expensive behaviours.The DEE–RMR slope was different at the among‐ versus within‐individual levels, with values supporting the performance and allocation models at the among‐ and within‐individual levels, respectively. Accordingly, the relationship between voluntary wheel running and RMR was positive at the among‐individual level (r = 0.40 ± 0.21), but negative at the within‐individual level (r = −0.23 ± 0.10).To our knowledge, this is the first study to simultaneously partition the relationship between RMR and behaviour at the among‐ versus within‐individuals levels while determining which energy management models apply at each of these levels. In doing so, we have identified a mechanism through which compensation occurs at the within‐individual level. A free Plain Language Summary can be found within the Supporting Information of this article. [ABSTRACT FROM AUTHOR]

Background. Diabetes is a chronic and progressive disease affecting all areas of life. It requires not only pharmacological treatment, but more importantly lifestyle changes, weight reduction, and dietary modifications. Improperly treated, it causes numerous complications that can lead to disability and even death. Material and methods. This study aimed to evaluate the effect health behaviors have on metabolic compensation in patients with type 2 diabetes. The study consisted of 116 patients. The inclusion criteria included type 2 diabetics between the ages of 40 and 65 who were diagnosed by a diabetologist for a minimum of one year. The KomPAN questionnaire, PSS 10 scales, International Physical Activity Questionnaire (IPAQ), and analysis of medical records were used to evaluate these effects. Of the 116 patients, 104 (54 women and 50 men) met the inclusion criteria and were used in data analysis. Results. No patient in our study met all the criteria for metabolic compensation of type 2 diabetes. Postprandial glucose concentrations were the best-compensated parameter. Whereas, LDL concentrations were the least compensated parameter. In individuals with fewer unhealthy dietary practices compensated more significantly for their diabetes. Seventy-eight percent of women and 90% of men with BMIs consistent with stages I and II overweight or obesity had abnormal fasting glucose levels. Conclusions. The factors that significantly impact diabetes compensation are diet, stress levels, and physical activity levels. The assessment of a patient's nutritional knowledge correlates with their dietary assessment. [ABSTRACT FROM AUTHOR]

Rare subpopulations of cancer stem cells (CSCs) have the ability to self-renew and are the primary driving force behind cancer metastatic dissemination and the preeminent hurdle to cancer treatment. As opposed to differentiated, non-malignant tumor offspring, CSCs have sophisticated metabolic patterns that, depending on the kind of cancer, rely mostly on the oxidation of major fuel substrates such as glucose, glutamine, and fatty acids for survival. Glutaminolysis is a series of metabolic reactions that convert glutamine to glutamate and, eventually, α-ketoglutarate, an intermediate in the tricarboxylic acid (TCA) cycle that provides biosynthetic building blocks. These building blocks are mostly utilized in the synthesis of macromolecules and antioxidants for redox homeostasis. A recent study revealed the cellular and molecular interconnections between glutamine and cancer stemness in the cell. Researchers have increasingly focused on glutamine catabolism in their attempt to discover an effective therapy for cancer stem cells. Targeting catalytic enzymes in glutaminolysis, such as glutaminase (GLS), is achievable with small molecule inhibitors, some of which are in early-phase clinical trials and have promising safety profiles. This review summarizes the current findings in glutaminolysis of CSCs and focuses on novel cancer therapies that target glutaminolysis in CSCs.

Hiroyoshi Taketani,1,* Taichiro Nishikawa,1,* Hisakazu Nakajima,2 Kazuki Kodo,2 Satoru Sugimoto,2 Wataru Aoi,3 Shin-ichi Horike,4 Makiko Meguro-Horike,4 Hiroshi Ishiba,1 Yuya Seko,1 Atsushi Umemura,1 Kanji Yamaguchi,1 Michihisa Moriguchi,1 Kohichiroh Yasui,1 Yoshito Itoh11Department of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, Japan; 2Department of Pediatrics, Kyoto Prefectural University of Medicine, Kyoto, Japan; 3Division of Applied Life Sciences, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto, Japan; 4Advanced Science Research Center, Kanazawa University, Kanazawa, Japan*These authors contributed equally to this workCorrespondence: Taichiro NishikawaKyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachidouri Hirokouji Agaru, Kamigyo-ku, Kyoto 602-8566, JapanTel +81 75 251 5519Fax +81 75 251 1017Email taichi@koto.kpu-m.ac.jpBackground and aims: Nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome, and its progression is associated with aging-associated impairment in metabolic homeostasis. Recently, energy metabolism in adipose tissue has been the subject of renewed interest, because significant energy expenditure can be induced in cells derived from white adipose tissue progenitors, in addition to brown adipose tissue (BAT). Here we evaluated whether aging-associated change in various adipose tissue depots affects the progression of NAFLD.Methods: Six-week-old male C57BL/6NCrSlc mice were fed control chow (C) or high-fat diet (60% fat; HF) for 12 or 24 weeks (12w/C, 12w/HF, 24w/C and 24w/HF groups, respectively) or switched from C to HF diet at 18 weeks of age (24w/C/HF group) and fed for a further 24 weeks. Some 24w/HF mice received a subcutaneous transplantation of adipose progenitors (106, cells/mouse) from young donor mice. Basal energy expenditure, glucose tolerance, and liver and adipose tissue histology were then evaluated. In addition, features of senescence and the capacity of adipose progenitors to “brown” were compared in mice of various ages.Results: 12w/HF mice demonstrated compensation in the forms of hypertrophy of interscapular classical BAT and the appearance of subcutaneous beige adipocytes, consistent with improved metabolic homeostasis. In contrast, 24w/HF and 24w/C/HF mice developed obesity, glucose intolerance, and severe NAFLD, with accelerated senescence and loss of adipose progenitors in subcutaneous fat tissues. Recruitment of adipose progenitors ameliorated these findings in 24w/HF mice.Conclusion: Impaired metabolic compensation in adipose tissue resulted in the progression of NAFLD, which was associated with aging-related deterioration in adipose progenitors. A new approach targeting adipose tissue progenitors might represent a potential strategy for the prevention of NAFLD.Keywords: nonalcoholic fatty liver disease, obesity, scenescence, brown adipocyte, mesenchymal stem cells, cell transplantation

The Chinese giant salamander (Andrias davidianus), one of the largest extant amphibian species, has dramatically declined in the wild. As an ectotherm, it may be further threatened by climate change. Therefore, understanding the thermal physiology of this species should be the priority to formulate related conservation strategies. In this study, the plasticity in metabolic rate and thermal tolerance limits of A. davidianus larvae were studied. Specifically, the larvae were acclimated to three temperature levels (7 °C, cold stress; 15 °C, optimum; and 25 °C, heat stress) and two diet items (red worm or fish fray) for 20 days. Our results indicated that cold-acclimated larvae showed increased metabolic capacity, while warm-acclimated larvae showed a decrease in metabolic capacity. These results suggested the existence of thermal compensation. Moreover, the thermal tolerance windows of cold-acclimated and warm-acclimated larvae shifted to cooler and hotter ranges, respectively. Metabolic capacity is not affected by diet but fish-fed larvae showed superiority in both cold and heat tolerance, potentially due to the input of greater nutrient loads. Overall, our results suggested a plastic thermal tolerance of A. davidianus in response to temperature and diet variations. These results are meaningful in guiding the conservation of this species.

Introduction: Airway pressure in the first 100 ms of an occluded inspiration (P0.1) evaluates respiratory center activity. Its increase compensates for respiratory muscle weakness in amyotrophic lateral sclerosis (ALS). We aimed to evaluate if an exhaustion over disease progression emerges. Methods: Consecutive ALS patients with P0.1 at baseline (T0) above 90th percentile for the whole population were included. There were two patient categories within this population: G1 patients had respiratory function tests (RFT) at T0 and 6 months later (T1); G2 patients were immediately adapted to noninvasive ventilation at T0. Functional ALS rating scale (ALSFRS) and its subscores, RFT including maximal inspiratory pressure (MIP), P0.1 percentage (%P0.1), P0.1/MIP, blood gas analyses, phrenic nerve motor amplitude and nocturnal pulsed oximetry (NPO) were compared at T0 between groups (Mann–Whitney U test) and longitudinal progression in G1 was assessed (Wilcoxon test). p < 0.05 was taken as significant. Results: Forty-nine patients were studied: 13 men, mean disease duration 17.1 ± 19.5 months, 21 with spinal-onset; 27 bulbar-onset; one with respiratory presentation. In G1, there was a progressive deterioration in all variables but P0.1/MIP did not significantly change (p = 0.394). PCO2 (p = 0.045) and bicarbonate ion (HCO3−p = 0.054) increased. In G2, the ALSFRS (p = 0.049) scores were lower, PCO2 (p = 0.057) and HCO3− (p = 0.016) higher, and reduced arterial oxygen saturation (SpO2<90%) at NPO (p = 0.007). Discussion: Patients with high central respiratory drive responses did not develop a short-term "exhaustion phenomenon". Both metabolic and central respiratory mechanisms interact to compensate for respiratory muscle weakness. The role of spasticity and the respiratory-metabolic-renal buffering system deserves further studies. [ABSTRACT FROM AUTHOR]

Photocatalytic disinfection has long been used to combat pathogenic bacteria. However, the specific mechanism underlying photocatalytic disinfection and its corresponding targets remain unclear. In this study, an analysis of the potential mechanism underlying photocatalytic disinfection was performed based on integrated metabolic networks and transcriptional data. Two sets of RNA-seq data (wild type and a photocatalysis-resistant mutant mediated by titanium dioxide (TiO 2)) were processed to constrain the genome scale metabolic models (GSMM) of E. coli. By analyzing the metabolic network, the differential metabolic flux of every reaction was computed in constrained GSMM, and several significantly differential metabolic fluxes in reactions were extracted and analyzed. Most of these reactions were involved in the transmembrane transport of substances and occurred on the inner membrane or were an important component of the cell membrane. These results, which are consistent with the reported information, validated our analysis process. In addition, our work also identified other new and valuable metabolic pathways, such as the reaction ALCD2x, which has a great effect on the energy production process under bacterial anaerobic conditions. The DHAK reaction is also related to the metabolic process of ATP. These reactions with large differential metabolic fluxes merit further research. Additionally, to provide a strategy to address photocatalysis-resistant mutant bacteria, a metabolic compensation analysis was also performed. The metabolic compensation analysis results provided suggestions for a combined method that can effectively combat resistant bacteria. This method could also be used to explore the mechanisms of drug resistance in other microorganisms. Image 1 [ABSTRACT FROM AUTHOR]

For over a century, the hypothesis of temperature compensation, the maintenance of similar biological rates in species from different thermal environments, has remained controversial. An alternative idea, that fitness is greater at higher temperatures (the thermodynamic effect), has gained increasing traction. This alternative hypothesis is also being used to understand large-scale biodiversity responses to environmental change. Yet evidence in favour of each of these contrasting hypotheses continues to emerge. In consequence, the fundamental nature of organismal thermal responses and its implications remain unresolved. Here, we investigate these ideas explicitly using a global dataset of 619 observations of four categories of organismal performance, spanning 14 phyla and 403 species. In agreement with both hypotheses, we show a positive relationship between the temperature of maximal performance rate (Topt) and environmental temperature (Tenv) for developmental rate and locomotion speed, but not growth or photosynthesis rate. Next, we demonstrate that relationships between Tenv and the maximal performance rate (Umax) are rarely significant and positive, as expected if a thermodynamic effect predominates. By contrast, a positive relationship between Topt and Umax is always present, but markedly weaker than theoretically predicted. These outcomes demonstrate that while some form of thermodynamic effect exists, ample scope is present for biochemical and physiological adaptation to thermal environments in the form of temperature compensation. [ABSTRACT FROM AUTHOR]

Abstract: Environmentally cued hatching allows embryos to alter the time of hatching in relation to environment through phenotypic plasticity. Spatially variable temperatures within shallow nests of many freshwater turtles cause asynchronous development of embryos within clutches, yet neonates still hatch synchronously either by hatching early or via metabolic compensation. Metabolic compensation and changes in circadian rhythms presumably enable embryos to adjust their developmental rates to catch up to more advanced embryos within the nest. Hatchlings of the North American freshwater turtle Chrysemys picta usually overwinter within the nest and emerge the following spring, but still hatch synchronously via hatching early. Here, we used rates of oxygen consumption and heart rate profiles to investigate the metabolic rates of clutches of C. picta developing in conditions that result in asynchronous development to determine if compensatory changes in metabolism occur during incubation. Embryos hatched synchronously and displayed circadian rhythms throughout incubation, but exhibited no evidence of metabolic compensation. Phenotypic traits of hatchlings, including body size and righting performance, were also not affected by asynchronous development. We conclude that less developed embryos of C. picta hatch synchronously with their clutch‐mates by hatching early, which does not appear to inflict a fitness cost to individuals. The ultimate mechanism for synchronous hatching in C. picta could be for hatchlings to ensure an optimal overwintering position within the center of the nest. Consequently, immediate fitness costs will not hinder hatchling survival. The geographic location, as well as environmental and genetic factors unique to populations, can all influence hatching behavior in turtles through phenotypic plasticity. Hence, synchronous hatching is an adaptive bet‐hedging strategy in turtles, but the mechanisms to achieve it are diverse. [ABSTRACT FROM AUTHOR]

Introduction: The goal of the study was to determine the level of metabolic compensation expressed by glycosylated hemoglobin, fasting plasma glucose, and postprandial glucose as determined after a standardized breakfast; further, to evaluate interrelationships between the studied parameters and postprandial glucose levels. Methods: The study included 1055 patients with type 2 diabetes mellitus. Their fasting plasma glucose and postprandial glucose were measured before and after a standardized breakfast. Attending diabetologists completed a uniform questionnaire that included demographic data, type of antidiabetic treatment, duration of diabetes, latest glycosylated hemoglobin value, presence of dyslipidemia, and organic complications. Results: Glycosylated hemoglobin <53 mmol/ mol was achieved in 363 (34.2%), postprandial glucose < 7.5 mmol/l in 211 (19.9%), and fasting plasma glucose <6 mmol/l in 251 (23.7%) patients. Excellent metabolic compensation, indicated by all the above mentioned glycosylated hemoglobin, fasting plasma glucose, and postprandial glucose values simultaneously, was achieved in only 71 (6.7%) patients. Comparable to fasting plasma glucose and postprandial glucose values, correlation with glycosylated hemoglobin levels is statistically significant; however, there is no difference at different glycosylated hemoglobin levels. There was a significant correlation between dyslipidemia and postprandial glycemia (p = 0.013). Conclusion: The objective of care for patients with diabetes mellitus is to improve their longterm metabolic compensation; to that end, both fasting plasma glucose and postprandial glucose deserve equal attention. [ABSTRACT FROM AUTHOR]

Multigenic families are widely represented in the genomes of higher plants, and are required for the reliability of cellular functions. Damage of individual genes can be compensated by diverse metabolic alterations, but the exact mechanisms of such compensations still remain not fully understood. Here we present novel data regarding the mechanisms of metabolic compensation in photorespiratory knock-out mutants cat2, cat3 and cat2cat3 of Arabidopsis thaliana, which are lacking activity of catalase isoforms CAT2 and CAT3. It was found that cultivation of the mutants under low light at optimal or increased temperature did not result in any morphological, physiological or biochemical signs of oxidative stress. Each of the mutant lines shows specific features of the compensatory mechanisms. Increased activity of CAT3 isoenzyme was found in the cat2 mutant, whereas cat3 and cat2cat3 demonstrate induction of CAT1, an isoform normally absent in young leaves, as well as activation of peroxidases, namely APX and POD. Comparison of these results and earlier published data revealed that the lack of CAT2 and CAT3 isoforms is compensated by preferential activation of non-enzymatic and enzymatic protection mechanisms, respectively. [ABSTRACT FROM AUTHOR]

Hypoxia is common in aquatic environments and has substantial effects on development, metabolism and survival of aquatic organisms. To understand the physiological effects of hypoxia and its dependence on temperature, metabolic rate ( M ̇ O 2 ) and cardiorespiratory function were studied in response to acute hypoxia (21 → 5 kPa) at different measurement temperatures (T a ; 4, 8 and 12 °C) in Salmo salar alevins that were incubated under normoxic conditions (P O 2 = 21 kPa) or following hypoxic acclimation (P O 2 = 10 kPa) as well as two different temperatures (4 °C or 8 °C). Hypoxic acclimation lead to a developmental delay manifested through slower yolk absorption. The general response to acute hypoxia was metabolic depression (~ 60%). Hypoxia acclimated alevins had higher M ̇ O 2 s when measured in normoxia than alevins acclimated to normoxia. M ̇ O 2 s were elevated to the same degree (~ 30% per 4 °C change) irrespective of T a . Under severe, acute hypoxia (~ 5 kPa) and irrespective of T a or acclimation, M ̇ O 2 s were similar between most groups. This suggests that despite different acclimation regimes, O 2 transport was limited to the same degree. While cardiorespiratory function (heart-, ventilation rate) was unchanged in response to acute hypoxia after normoxic acclimation, hypoxic acclimation led to cardiorespiratory changes predominantly in severe hypoxia, indicating earlier onset and plasticity of cardiorespiratory control mechanisms. Although M ̇ O 2 in normoxia was higher after hypoxic acclimation, at the respective acclimation P O 2 , M ̇ O 2 was similar in normoxia and hypoxia acclimated alevins. This is indicative of metabolic compensation to an intrinsic M ̇ O 2 at the acclimation condition in hypoxia-acclimated alevins after re-exposure to normoxia. [ABSTRACT FROM AUTHOR]

ABSTRACT Viruses are believed to be responsible for the mortality of host organisms. However, some recent investigations reveal that viruses may be essential for host survival. To date, it remains unclear whether viruses are beneficial or harmful to their hosts. To reveal the roles of viruses in the virus-host interactions, viromes and microbiomes of sediment samples from three deep-sea hydrothermal vents were explored in this study. To exclude the influence of exogenous DNAs on viromes, the virus particles were purified with nuclease (DNase I and RNase A) treatments and cesium chloride density gradient centrifugation. The metagenomic analysis of viromes without exogenous DNA contamination and microbiomes of vent samples indicated that viruses had compensation effects on the metabolisms of their host microorganisms. Viral genes not only participated in most of the microbial metabolic pathways but also formed branched pathways in microbial metabolisms, including pyrimidine metabolism; alanine, aspartate, and glutamate metabolism; nitrogen metabolism and assimilation pathways of the two-component system; selenocompound metabolism; aminoacyl-tRNA biosynthesis; and amino sugar and nucleotide sugar metabolism. As is well known, deep-sea hydrothermal vent ecosystems exist in relatively isolated environments which are barely influenced by other ecosystems. The metabolic compensation of hosts mediated by viruses might represent a very important aspect of virus-host interactions. IMPORTANCE Viruses are the most abundant biological entities in the oceans and have very important roles in regulating microbial community structure and biogeochemical cycles. The relationship between virus and host microbes is broadly thought to be that of predator and prey. Viruses can lyse host cells to control microbial population sizes and affect community structures of hosts by killing specific microbes. However, viruses also influence their hosts through manipulation of bacterial metabolism. We found that viral genes not only participated in most microbial metabolic pathways but also formed branched pathways in microbial metabolisms. The metabolic compensation of hosts mediated by viruses may help hosts to adapt to extreme environments and may be essential for host survival.

Most experiments examining acid-base regulation of chicken embryos have employed static, single time point measurements rather than dynamic, multiple time point measurements that might reveal additional components of developing acid-base regulation. Thus, we studied blood acid-base balance and hematology of day 15 chicken embryos under 24 h exposure to graded hypercapnia (1%–7% CO 2 ) accompanied by graded hypoxia (20% O 2 down to 13% O 2 ). Across all hypercapnic/hypoxic environments, respiratory acidosis occurred 2 h after exposure in proportion to the magnitude of hypercapnia. An additional metabolic alkalosis occurred in ≥16% O 2 , and metabolic acidosis in ≤14% O 2 . As exposure progressed, compensatory metabolic alkalosis occurred in all groups at 6 h, but partial metabolic compensation could not be preserved as hypoxia increased (≤18% O 2 ). Across all hypercapnic/hypoxic groups, hematocrit, mean corpuscular volume and red blood cell concentration significantly increased by 24 h, most likely due to hypoxia rather than hypercapnia. Overall, day 15 chicken embryos cannot maintain even partial compensation in their acid-base physiology after 24 h exposure to hypercapnic/hypoxic environments of ≥5% CO 2 + ≤15% O 2 . [ABSTRACT FROM AUTHOR]

Introduction: In aspect of the influence of quantity and quality of sleep on metabolic control of type 1 diabetes (T1D) the works extended in last years, but data are limited in childhood. In 2016 meta-analysis revealed that children with type 1 diabetes slept shorter than their peers. Conclusions were not done in aspect of sleep quality and presence of sleep disordered breathing. Goal: The aim of work was to examine sleep quality by polysomnographic examination in the group of children with type 1 diabetes and to determine the influence of short-term and long-term metabolic compensation (HbA1c) on sleep quality in children with type 1 diabetes. Methods: 44 children (28 girls and 16 boys) aged 10-18 years with type 1 diabetes were included to the study after exclusion of children with hypoglycemia before and during polysomnography. The group was divided into two subgroups, The first group (n=23) consisted from children with sub-optimal metabolic control of diabetes (HbA1c 7.5-9%), while children with non-optimal control of diabetes (HbA1c *9%) were included to the second group. The subgroups did not differ in aspect of anthropometric parameters and diabetes duration. Results of continuous glucose monitoring and polysomnographic examinations were analysed in subgroups. Results: We did not find significant difference in parameters of sleep latency, sleep effectivity, percentage of time spended in NREM N1, NREM N3, AHI and OAHI. Children with worse metabolic control of type 1 diabetes (HbA1c *9%) spent significantly more time in sleep stage of NREM N2 (51.352% vs. 45.565%, p=0.008), significantly less time in sleep stage of REM (15.990% vs. 19.052%, p=0.011) and had significantly lower effectivity of deep sleep (45.114% vs. 49.913%, p=0.028) comparing to children with long-term better metabolic control of diabetes. Obstructive sleep apnoe (OSA) was diagnosed in only one patient, 9 children had mild degree of central sleep disordered breathing. Conclusion: Children with non-optimal metabolic control of T1D spent more time in sleep stage of NREM N2 and had significantly decreased effectivity of deep sleep NREM N3. Approximatelly one fifth of children with T1D had mild central disordered breathing, the prevalence of OSA was comparable with general pediatric population. We did not find difference in the occurance of sleep disordered breathing in relation to compensation of T1D in children and adolescents. [ABSTRACT FROM AUTHOR]

To examine whether metabolic compensation during seasonal acclimatization at the liver mitochondrial level is consistent with that at the whole-animal level, respiration rates of liver mitochondria and resting metabolic rates in winter- and summer- acclimatized southern catfish (Silurus meridionalis Chen) were measured. At 12.5, 17.5, 22.5, 27.5 and 32.5°C, the mean values of state 3 respiration rates were 12.21, 13.84, 18.96, 24.78 and 32.01 nmol O2 min-1 mg-1 mitochondrial protein in the winter group, and 8.56, 9.20, 17.32, 22.74 and 26.32 nmol O2 min-1 mg-1 in the summer group, respectively. At the five assay temperatures the resting metabolic rates were 24.86, 42.68, 61.59, 84.10 and 125.65 mg O2 h-1 kg-1 body mass in the winter group, and 22.89, 40.59, 52.94, 75.13 and 109.35 mg O2 h-1 kg-1 in the summer group, respectively. Total mitochondrial respiration rates in the liver organ were estimated based on state 3 respiration rates, mitochondrial protein content and organ mass, and the mean values were 72.96, 71.87, 112.47, 167.35 and 183.27 nmol O2 min-1 in the winter group, and were 47.89, 47.39, 105.67, 138.18 and 132.29 nmol O2 min-1 in the summer group, respectively. Metabolic compensation caused by seasonal acclimatization occurred at the liver mitochondrial level and compensation at the liver organ level was found to be more efficient because of an increase in metabolic capacity of mitochondria and a boost in organ mass. Metabolic compensation at the whole-animal level was not detected. During seasonal acclimatization, the effect of metabolic compensation at liver mitochondrial level is inconsistent with that at the whole-animal level in the southern catfish. This may be due to different degrees of regulation of metabolic mechanisms among various tissues and organs in an acclimatized organism [Current Zoology 57 (1): 109–115, 2011].

Variable temperatures within a nest cause asynchronous development within clutches of freshwater turtle embryos, yet synchronous hatching occurs and is thought to be an important survival strategy for hatchlings. Metabolic compensation and circadian rhythms in heart rates of embryonic turtles indicate the potential of communication between embryos in a nest. Heart rates were used to identify metabolic circadian rhythms in clutches of an Australian freshwater turtle ( Chelodina longicollis ) and determine whether embryos metabolically compensate and hatch synchronously when incubated in asynchronous environments. The effects of a group environment during incubation on egg development and incubation period were also investigated during the final 3 weeks of development. Chelodina longicollis hatch synchronously and metabolically compensate so that less advanced embryos catch up to more advanced clutch-mates. Heart rates of embryos remained stable from week 4–7 in asynchronous (M = 89 bpm) and synchronous (M = 92 bpm) groups and declined in the final 2 weeks of incubation (M = 72 and 77 bpm). Circadian rhythms were present throughout development and diel heart rates of embryos in asynchronous groups showed less deviation from the mean (M = − 0.5 bpm) than synchronous groups (M = − 4 bpm). Eggs incubated in groups had a significantly shorter incubation period than eggs incubated individually. Phenotypic traits including size, performance, and growth of all hatchlings were not affected. Egg position within a turtle nest is important for coordinating development throughout incubation and facilitating synchronous hatching. [ABSTRACT FROM AUTHOR]

Time specific acid–base metabolic compensation and responses of hematological respiratory variables were measured in day 15 layer (Hyline) and broiler (Cornish Rock) chicken embryos during acute hypercapnic challenges (3, 6, 10 and 20% CO 2 ). Control acid–base status and hematology differed between two strains. Broiler embryos were relatively respiratory acidotic and had higher hematocrit (Hct) and hemoglobin concentration. The partial metabolic compensation for respiratory acidosis produced by ≤10% CO 2 exposures occurred in proportion to CO 2 concentrations in both strains, but metabolic compensation for 20% CO 2 respiratory acidosis was depressed at 2, 6 and 24 h, particularly in broiler embryos. Exposure to ≤10% CO 2 induced the same hematological responses across CO 2 concentrations; i.e., Hct and mean corpuscular volume (MCV) increased while RBC concentration remained unchanged. In response to 20% CO 2 exposure, Hct and MCV increased dramatically in both stains. Consequently, altered acid–base and hematology responses to 20% CO 2 exposure compared to ≤10% CO 2 suggest that the hypercapnic threshold to compensation for acidosis and regulation of hematology is >10% CO 2 . [ABSTRACT FROM AUTHOR]

In order to examine the effects of seasonal acclimation on mitochondrial metabolic functions and test tissue-specific pattern of the metabolic compensation within individuals of the southern catfish ( Silurus meridionalis Chen), rates of mitochondrial respiration and activities of cytochrome c oxidase (COX) in the heart, liver, kidney, brain and white muscle of this fish in the summer-acclimatized group (153.20 ± 1.66 g) and winter-acclimatized group (177.71 ± 3.04 g) were measured at seven assay temperatures (7.5, 12.5, 17.5, 22.5, 27.5, 32.5 and 37.5 °C), respectively. The results show that compensatory adjustments in state III respiratory rate and COX activity occur significantly in the heart, kidney and liver, but do not in the brain and white muscle, which suggest that the metabolic compensation of this fish in response to seasonal acclimation exhibits a tissue-specific pattern. The cold acclimation increases mitochondrial oxidative capacities in the heart, kidney and liver concomitantly with reducing their upper thermal limits of mitochondrial functions at acute warming and the thermal tolerance shifts in the same tissue-specific pattern as the metabolic compensation. When combining the effects of seasonal acclimation on mitochondrial oxidative capacity and organ mass, the metabolic compensation demonstrates an organ-specific pattern with four categories: over-compensation in the heart, complete compensation in the kidney, partial compensation in the liver and no compensation in the brain. The organ-specific pattern of metabolic compensation might be a trade-off strategy of the performance adjustments in the seasonal acclimation for this fish to maximize its fitness. [ABSTRACT FROM AUTHOR]

The acquisition of fertilizing ability by mammalian spermatozoa, known as "capacitation," includes processes that depend on particular metabolic pathways. This has led to the hypothesis that ATP demands might differ between capacitated and non-capacitated cells. Mouse sperm can produce ATP via OXPHOS and aerobic glycolysis, an advantageous characteristic considering that these cells have to function in the complex and variable environment of the female reproductive tract. Nonetheless, despite evidence showing that both metabolic pathways play a role in events associated with mouse sperm capacitation, there is contradictory evidence regarding changes promoted by capacitation in this species. In addition, the vast majority of studies regarding murine sperm metabolism use Mus musculus laboratory strains as model, thus neglecting the wide diversity of sperm traits of other species of Mus. Focus on closely related species with distinct evolutionary histories, which may be the result of different selective pressures, could shed light on diversity of metabolic processes. Here, we analyzed variations in sperm bioenergetics associated with capacitation in spermatozoa of the steppe mouse, Mus spicilegus, a species with high sperm performance. Furthermore, we compared sperm metabolic traits of this species with similar traits previously characterized in M. musculus. We found that the metabolism of M. spicilegus sperm responded to capacitation in a manner similar to that of M. musculus sperm. However, M. spicilegus sperm showed distinct metabolic features, including the ability to perform cross-pathway metabolic compensation in response to either respiratory or glycolytic inhibition, thus revealing a delicate fine-tuning of its metabolic capacities., (© 2022. The Author(s).)

Simple Summary: The Chinese giant salamander (Andrias davidianus) is one of the largest extant amphibian species, and it is considered critically endangered by the IUCN Red List. Previous studies have demonstrated that future climate change could strongly affect this species. However, how to conduct the related conservation activities are still unclear. Understanding the thermal physiology of A. davidianus is meaningful in guiding its conservation, e.g., habitat selection and preadaptation before population translocation. In this study, the influences of temperature and diet on the metabolic capacity and thermal limits were studied for A. davidianus larvae based on laboratory experiments. Our results indicated prominent physiological plasticity in the thermal tolerance of A. davidianus in response to temperature and diet changes. This thermal plasticity likely, to some extent, buffers the effects of climate change on the Chinese giant salamander. In addition, the potential mechanisms underlying this plasticity were discussed. Our results provide insights for the formulation of conservation strategies for this species. The Chinese giant salamander (Andrias davidianus), one of the largest extant amphibian species, has dramatically declined in the wild. As an ectotherm, it may be further threatened by climate change. Therefore, understanding the thermal physiology of this species should be the priority to formulate related conservation strategies. In this study, the plasticity in metabolic rate and thermal tolerance limits of A. davidianus larvae were studied. Specifically, the larvae were acclimated to three temperature levels (7 °C, cold stress; 15 °C, optimum; and 25 °C, heat stress) and two diet items (red worm or fish fray) for 20 days. Our results indicated that cold-acclimated larvae showed increased metabolic capacity, while warm-acclimated larvae showed a decrease in metabolic capacity. These results suggested the existence of thermal compensation. Moreover, the thermal tolerance windows of cold-acclimated and warm-acclimated larvae shifted to cooler and hotter ranges, respectively. Metabolic capacity is not affected by diet but fish-fed larvae showed superiority in both cold and heat tolerance, potentially due to the input of greater nutrient loads. Overall, our results suggested a plastic thermal tolerance of A. davidianus in response to temperature and diet variations. These results are meaningful in guiding the conservation of this species. [ABSTRACT FROM AUTHOR]

CO exposure elicits multiple changes in the acid-base balance and hematology of avian embryos, but the time-specific, dose-dependent effects of graded increases in extrinsic CO in a normoxic environment are poorly understood. Consequently, we exposed day 15 chicken embryos to 1, 3, 5, 6 or 10 % CO in 20 % O. We hypothesized that both the magnitude of hypercapnic respiratory acidosis and the resultant metabolic compensation within 24 h of exposure to <10 % CO are proportional to ambient CO concentration ([CO]). We also predicted that regulation of hematological respiratory variables is graded according to [CO]. Time-course (2, 6 and 24 h) changes were determined for acid-base disturbances and hematological respiratory variables; hematocrit (Hct), red blood cell concentration ([RBC]), hemoglobin concentration, mean corpuscular volume (MCV) and other mean corpuscular indices. Both the decrease in uncompensated pH, which indicates uncompensated respiratory acidosis, and the compensatory pH increase, a sign of metabolic compensation, increased with [CO]. The partial metabolic compensation across all CO gas mixtures was ~17, 46 and 53 % compensation at 2, 6 and 24 h, respectively. Hematological responses were nearly identical across the entire range of [CO], with Hct decreasing across the time course of CO exposure due to a decrease in MCV from 2 to 24 h and a decrease in [RBC] at 24 h. Even though hematological regulation was not graded, chicken embryos were able to compensate and survive exposure to <10 % CO. [ABSTRACT FROM AUTHOR]

Background: Gene expression regulation is one of the fundamental mechanisms of phenotypic plasticity and is expected to respond to selection in conditions favoring phenotypic response. The observation that many organisms increase their stress tolerance after acclimation to moderate levels of stress is an example of plasticity which has been long hypothesized to be based on adaptive changes in gene expression. We report genome-wide patterns of gene expression in two heat-tolerant and two heat-sensitive parthenogenetic clones of the zooplankton crustacean Daphnia pulex exposed for three generations to either optimal (18°C) or substressful (28°C) temperature. Results: A large number of genes responded to temperature and many demonstrated a significant genotype-by-environment (GxE) interaction. Among genes with a significant GxE there were approximately equally frequent instances of canalization, i.e. stronger plasticity in heat-sensitive than in heat-tolerant clones, and of enhancement of plasticity along the evolutionary vector toward heat tolerance. The strongest response observed is the across-the-board down-regulation of a variety of genes occurring in heat-tolerant, but not in heat-sensitive clones. This response is particularly obvious among genes involved in core metabolic pathways and those responsible for transcription, translation and DNA repair. Conclusions: The observed down-regulation of metabolism, consistent with previous findings in yeast and Drosophila, may reflect a general compensatory stress response. The associated down-regulation of DNA repair pathways potentially creates a trade-off between short-term benefits of survival at high temperature and long-term costs of accelerated mutation accumulation. [ABSTRACT FROM AUTHOR]

Embryos of Austrofundulus limnaeus are exceptional in their ability to tolerate prolonged bouts of complete anoxia. Hypoxia and anoxia are a normal part of their developmental environment. Here, we exposed embryos to a range of PO levels at two different temperatures (25 and 30 °C) to study the combined effects of reduced oxygen and increased temperature on developmental rate, heart rate, and metabolic enzyme capacity. Hypoxia decreased overall developmental rate and caused a stage-specific decline in heart rate. However, the rate of early development prior to the onset of organogenesis is insensitive to PO. Increased incubation temperature caused an increase in the developmental rate at high POs, but hindered developmental progression under severe hypoxia. Embryonic DNA content in pre-hatching embryos was positively correlated with PO. Citrate synthase, lactate dehydrogenase, and phosphoenolpyruvate carboxykinase capacity were all reduced in embryos developing under hypoxic conditions. Embryos of A. limnaeus are able to develop normally across a wide range of POs and contrary to most other vertebrates severe hypoxia is not a teratogen. Embryos of A. limnaeus do not respond to hypoxia through an increase in the capacity for enzymatic activity of the metabolic enzymes lactate dehydrogenase, citrate synthase, or phosphoenolpyruvate carboxykinase. Instead they appear to adjust whole-embryo metabolic capacity to match oxygen availability. However, decreased DNA content in hypoxia-reared embryos suggests that cellular enzymatic capacity may remain unchanged in response to hypoxia, and the reduced capacity may rather indicate reduced cell number in hypoxic embryos. [ABSTRACT FROM AUTHOR]

Abstract: In day 15 chicken embryos, we determined the time course responses of acid–base balance and hematological respiratory variables during 24h exposure to 15, 20, 40 or 90% O2, in the presence of 5% CO2. Hypercapnic respiratory acidosis was initially (2h) only slightly (∼20%) compensated by metabolic alkalosis in normoxic/hyperoxic embryos. After 6h, respiratory acidosis was partially (∼40–50%) compensated not only in normoxic/hyperoxic embryos, but also in hypoxic embryos. However, partial metabolic compensation in 15% O2 could not be preserved after 24h. Preservation of metabolic compensation required oxygen concentration ([O2]) above 20%, but the magnitude of partial metabolic compensation was unrelated to [O2]. Hematocrit (Hct), together with mean corpuscular volume (MCV), markedly increased in hypercapnic hypoxia, and was maintained at 24h due to a subsequent increase in red blood cell concentration ([RBC]). In contrast, Hct, together with MCV, decreased in hypercapnic normoxia/hyperoxia accompanied by a subsequent decrease in [RBC] at 24h. Regulation of variables takes place similarly irrespective of environmental [O2] above 20%, matching acid–base regulation. [Copyright &y& Elsevier]

Incubation temperature affects developmental rates and defines many phenotypes and fitness characteristics of reptilian embryos. In turtles, eggs are deposited in layers within the nest, such that thermal gradients create independent developmental conditions for each egg. Despite differences in developmental rate, several studies have revealed unexpected synchronicity in hatching, however, the mechanisms through which synchrony are achieved may be different between species. Here, we examine the phenomenon of synchronous hatching in turtles by assessing proximate mechanisms in an Australian freshwater turtle (Emydura macquarii). We tested whether embryos hatch prematurely or developmentally compensate in response to more advanced embryos in a clutch. We established developmental asynchrony within a clutch of turtle eggs and assessed both metabolic and heart rates throughout incubation in constant and fluctuating temperatures. Turtles appeared to hatch at similar developmental stages, with less-developed embryos in experimental groups responding to the presence of more developed eggs in a clutch by increasing both metabolic and heart rates. Early hatching did not appear to reduce neuromuscular ability at hatching. These results support developmental adjustment mechanisms of the ‘catch-up hypothesis’ for synchronous hatching in E. macquarii and implies some level of embryo–embryo communication. The group environment of a nest strongly supports the development of adaptive communication mechanisms between siblings and the evolution of environmentally cued hatching. [ABSTRACT FROM AUTHOR]

Nutritional deficiency in combination with drug abuse may increase risk of developing the metabolic syndrome by augmenting cell damage, excitotoxicity, reducing energy production, and lowering the antioxidant potential of the cells. We have reviewed here the following points: effects of drugs of abuse on nutrition and brain metabolism; effects of nutrition on actions of the drugs of abuse; drug abuse and probability of developing metabolic syndrome; role of genetic vulnerability in nutrition/drug abuse and brain damage; and the role of neuroprotective supplements in drug abuse. Nutrition education is an essential component of substance abuse treatment programs and can enhance substance abuse treatment outcomes. The strategies available, in particular the nutritional approach to protect the drug abusers from the metabolic syndrome and other diseases are discussed. [ABSTRACT FROM AUTHOR]

The capacity of tropical whitespotted bamboo sharks Chiloscyllium plagiosum to metabolically compensate, at both the whole-animal and biochemical levels, to prolonged exposure to temperatures higher (30° C) and lower (20 and 15° C) than their native temperature (24·5° C) was examined. As expected, whitespotted bamboo shark oxygen consumption increased upon exposure to 30° C and decreased at 20 and 15° C. Initial changes in oxygen consumption were maintained even after months at the experimental temperature, indicating that whitespotted bamboo sharks did not compensate metabolically to the experimental temperatures. Maximal activities and thermal sensitivity of citrate synthase and lactate dehydrogenase from whitespotted bamboo shark white locomotor muscle were similar between control animals maintained at 24·5° C and those maintained at 15° C, indicating that cold-exposed animals did not compensate at the biochemical level. Similarly, lactate dehydrogenase activity did not change following prolonged exposure to 30° C. White muscle from whitespotted bamboo sharks maintained at 30° C had significantly lower citrate synthase activity than did control animals. This result was surprising given the lack of metabolic compensation at the whole-animal level. Overall, whole-animal oxygen consumption measurements supported the hypothesis that animals from thermally stable environments lacked the capacity to metabolically compensate to altered temperatures. Enzymatic results, however, suggested that the metabolic potential of muscle could change following temperature acclimation even in the absence of metabolic compensation at the whole-animal level. [ABSTRACT FROM AUTHOR]

The swamp eel ( Monopterus albus ) uses its buccal cavity to air breathe, while the gills are strongly reduced. It burrows into mud during the dry season, is highly tolerant of air exposure, and experiences severe hypoxia both in its natural habitat and in aquaculture. To study the ability of M. albus to compensate for respiratory acidosis, we implanted catheters to sample both arterial blood and urine during hypercapnia (4% CO 2 ) in either water or air, or during whole-animal air exposure. These hypercapnic challenges caused an immediate reduction in arterial pH, followed by progressive compensation through a marked elevation of plasma HCO 3 - over the course of 72 h. There was no appreciable rise in urinary acid excretion in fish exposed to hypercapnia in water, although urine pH was reduced and ammonia excretion did increase. In the air-exposed fish, however, hypercapnia was attended by a large elevation of ammonia in the urine and a large rise in titratable acid excretion. The time course of the increased renal acid excretion overlapped with the time period required to elevate plasma HCO 3 - , and we estimate that the renal compensation contributed significantly to whole-body acid-base compensation., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2019. Published by The Company of Biologists Ltd.)

Viruses are believed to be responsible for the mortality of host organisms. However, some recent investigations reveal that viruses may be essential for host survival. To date, it remains unclear whether viruses are beneficial or harmful to their hosts. To reveal the roles of viruses in the virus-host interactions, viromes and microbiomes of sediment samples from three deep-sea hydrothermal vents were explored in this study. To exclude the influence of exogenous DNAs on viromes, the virus particles were purified with nuclease (DNase I and RNase A) treatments and cesium chloride density gradient centrifugation. The metagenomic analysis of viromes without exogenous DNA contamination and microbiomes of vent samples indicated that viruses had compensation effects on the metabolisms of their host microorganisms. Viral genes not only participated in most of the microbial metabolic pathways but also formed branched pathways in microbial metabolisms, including pyrimidine metabolism; alanine, aspartate, and glutamate metabolism; nitrogen metabolism and assimilation pathways of the two-component system; selenocompound metabolism; aminoacyl-tRNA biosynthesis; and amino sugar and nucleotide sugar metabolism. As is well known, deep-sea hydrothermal vent ecosystems exist in relatively isolated environments which are barely influenced by other ecosystems. The metabolic compensation of hosts mediated by viruses might represent a very important aspect of virus-host interactions. IMPORTANCE Viruses are the most abundant biological entities in the oceans and have very important roles in regulating microbial community structure and biogeochemical cycles. The relationship between virus and host microbes is broadly thought to be that of predator and prey. Viruses can lyse host cells to control microbial population sizes and affect community structures of hosts by killing specific microbes. However, viruses also influence their hosts through manipulation of bacterial metabolism. We found that viral genes not only participated in most microbial metabolic pathways but also formed branched pathways in microbial metabolisms. The metabolic compensation of hosts mediated by viruses may help hosts to adapt to extreme environments and may be essential for host survival., (Copyright © 2017 He et al.)

Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco 2 , increases in pH, and compensatory decreases in blood HCO 3 levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO - levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO 3 - and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO 3 - ; the arterial pH can approach near-normal values., (Copyright © 2016 Elsevier Inc. All rights reserved.)