Changes In Energy Stores Research Articles

How much do large whales eat?

Estimates of the amount of prey consumed by cetaceans have been used in ecological models and also directly compared to human fisheries yields. Most of these estimates have been based on assumptions about energy requirements. However, the lack of direct measurements for large whales has necessitated extrapolation beyond the data points available from smaller species. A number of different parameterisations of general regressions in which energy requirements or consumption are estimated as proportional to body mass raised to some power B, were compared with estimates of Basal Metabolic Rate (BMR) from the widely used Kleiber equation. The choice of values has a large impact on estimates, which can differ by an order of magnitude, but modellers are frequently forced to make rather arbitrary decisions due to lack of data. Nevertheless, neither data nor theory appear to support values of B >0.75. Although some parameter values have obtained status through common usage, these have not always been based on actual data and estimates of consumption by whales need to reflect this uncertainty. Comparison of generalised relationships with data from other sources, including rates of filter feeding, oxygen consumption and seasonal changes in energy stores, suggest upper bounds on average daily metabolic rate of large whales. Estimates based on stomach contents also indicated average daily metabolic rates of less than four times the BMR from the Kleiber formula, but these are critically dependent on estimates of digestion time for which there appear to be little data. Estimates of stored energy suggest that large whales that migrate to seasonally productive feeding areas either have relatively low energy requirements for their size or need to meet a considerable proportion of their annual energy requirements outside of the feeding grounds.

FKBP5/FKBP51 on weight watch: central FKBP5 links regulatory WIPI protein networks to autophagy and metabolic control

ABSTRACT Stress and changes in energy stores are perceived by hormone- and nutrient-sensing nuclei of the hypothalamus, which orchestrate an adaptive physiological body response to maintain homeostasis. Macroautophagy/autophagy is a fundamental lysosomal degradation system contributing to preservation of proteome balance and metabolic homeostasis. Its dysregulation is linked to diverse human pathologies, including neuropsychiatric and metabolic disorders. Autophagy is coordinated by cellular nutrient sensors, including AMPK and MTORC1 that interact with WIPI proteins. Studies suggest that WDR45/WIPI4 interacts with the stress-sensitive co-chaperone FKBP5/FKBP51, which has emerged as a key autophagy scaffold. However, the impact of FKBP5 on autophagy signaling in response to metabolic challenges, such as a high-fat diet, is elusive. Therefore, we manipulated FKBP5 in the mediobasal hypothalamus (MBH) and studied autophagy signaling and protein interactions in their physiological context. We identified FKBP5 as a scaffold of the STK11/LKB1-AMPK complex with WDR45/WIPI4 and TSC2 with WDR45B/WIPI3 in response to metabolic challenges, positioning FKBP5 in major nutrient-sensing and autophagy-regulating networks. Intriguingly, we could demonstrate that FKBP5 deletion in the MBH strongly induces obesity, whereas its overexpression protects against high-fat diet-induced obesity. Our findings suggest a crucial regulatory and adaptive function of FKBP5-regulated autophagy within the MBH in response to metabolic challenges. Abbreviations: AKT: thymoma viral proto-oncogene; AMPK: AMP-activated protein kinase; BECN1: beclin 1, autophagy related; eWAT: epididymal white adipose tissue; FKBP5/FKBP51: FK506 binding protein 5; KO, knockout; MBH, mediobasal hypothalamus; MTORC1, mechanistic target of rapamycin kinase complex 1; p: phosphorylated; PHLPP: PH domain and leucine rich repeat protein phosphatase; RPS6KB/p70S6K: ribosomal protein S6 kinase; SKP2: S-phase kinase-associated protein 2; SM: soleus muscle; SQSTM1/p62, sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TSC: TSC complex; ULK1: unc-51 like kinase 1; WIPI: WD repeat domain, phosphoinositide interacting; WT: wild type

Understanding the ecological and evolutionary function of stopover in migrating birds.

Global movement patterns of migratory birds illustrate their fascinating physical and physiological abilities to cross continents and oceans. During their voyages, most birds land multiple times to make so-called 'stopovers'. Our current knowledge on the functions of stopover is mainly based on the proximate study of departure decisions. However, such studies are insufficient to gauge fully the ecological and evolutionary functions of stopover. If we study how a focal trait, e.g. changes in energy stores, affects the decision to depart from a stopover without considering the trait(s) that actually caused the bird to land, e.g. unfavourable environmental conditions for flight, we misinterpret the function of the stopover. It is thus important to realise and acknowledge that stopovers have many different functions, and that not every migrant has the same (set of) reasons to stop-over. Additionally, we may obtain contradictory results because the significance of different traits to a migrant is context dependent. For instance, late spring migrants may be more prone to risk-taking and depart from a stopover with lower energy stores than early spring migrants. Thus, we neglect that departure decisions are subject to selection to minimise immediate (mortality risk) and/or delayed (low future reproductive output) fitness costs. To alleviate these issues, we first define stopover as an interruption of migratory endurance flight to minimise immediate and/or delayed fitness costs. Second, we review all probable functions of stopover, which include accumulating energy, various forms of physiological recovery and avoiding adverse environmental conditions for flight, and list potential other functions that are less well studied, such as minimising predation, recovery from physical exhaustion and spatiotemporal adjustments to migration. Third, derived from these aspects, we argue for a paradigm shift in stopover ecology research. This includes focusing on why an individual interrupts its migratory flight, which is more likely to identify the individual-specific function(s) of the stopover correctly than departure-decision studies. Moreover, we highlight that the selective forces acting on stopover decisions are context dependent and are expected to differ between, e.g. K-/r-selected species, the sexes and migration strategies. For example, all else being equal, r-selected species (low survival rate, high reproductive rate) should have a stronger urge to continue the migratory endurance flight or resume migration from a stopover because the potential increase in immediate fitness costs suffered from a flight is offset by the expected higher reproductive success in the subsequent breeding season. Finally, we propose to focus less on proximate mechanisms controlling landing and departure decisions, and more on ultimate mechanisms to identify the selective forces shaping stopover decisions. Our ideas are not limited to birds but can be applied to any migratory species. Our revised definition of stopover and the proposed paradigm shift has the potential to stimulate a fruitful discussion towards a better evolutionary ecological understanding of the functions of stopover. Furthermore, identifying the functions of stopover will support targeted measures to conserve and restore the functionality of stopover sites threatened by anthropogenic environmental changes. This is especially important for long-distance migrants, which currently are in alarming decline.

Warm acclimation alters antioxidant defences but not metabolic capacities in the Antarctic fish, Notothenia coriiceps.

The Southern Ocean surrounding the Western Antarctic Peninsula region is rapidly warming. Survival of members of the dominant suborder of Antarctic fishes, the Notothenioidei, will likely require thermal plasticity and adaptive capacity in key traits delimiting thermal tolerance. Herein, we have assessed the thermal plasticity of several cellular and biochemical pathways, many of which are known to be associated with thermal tolerance in notothenioids, including mitochondrial function, activities of aerobic and anaerobic enzymes, antioxidant defences, protein ubiquitination and degradation in cardiac, oxidative skeletal muscles and gill of Notothenia coriiceps warm acclimated to 4°C for 22 days or 5°C for 42 days. Levels of triacylglycerol (TAG) were measured in liver and oxidative and glycolytic skeletal muscles, and glycogen in liver and glycolytic muscle to assess changes in energy stores. Metabolic pathways displayed minimal thermal plasticity, yet antioxidant defences were lower in heart and oxidative skeletal muscles of warm-acclimated animals compared with animals held at ambient temperature. Despite higher metabolic rates at elevated temperature, energy storage depots of TAG and glycogen increase in liver and remain unchanged in muscle with warm acclimation. Overall, our studies reveal that N. coriiceps displays thermal plasticity in some key traits that may contribute to their survival as the Southern Ocean continues to warm.

Correlates of seasonal change in the body condition of an Arctic top predator.

Climate-driven sea ice loss has led to changes in the timing of key biological events in the Arctic, however, the consequences and rate of these changes remain largely unknown. Polar bears (Ursus maritimus) undergo seasonal changes in energy stores in relation to foraging opportunities and habitat conditions. Declining sea ice has been linked to reduced body condition in some subpopulations, however, the specific timing and duration of the feeding period when bears acquire most of their energy stores and its relationship to the timing of ice break-up is poorly understood. We used community-based sampling to investigate seasonality in body condition (energy stores) of polar bears in Nunavut, Canada, and examined the influence of sea ice variables. We used adipose tissue lipid content as an index of body condition for 1,206 polar bears harvested from 2010-2017 across five subpopulations with varying seasonal ice conditions: Baffin Bay (October-August), Davis Strait and Foxe Basin (year-round), Gulf of Boothia and Lancaster Sound (August-May). Similar seasonal patterns were found in body condition across subpopulations with bears at their nadir of condition in the spring, followed by fat accumulation past break-up date and subsequent peak body condition in autumn, indicating that bears are actively foraging in late spring and early summer. Late season feeding implies that even minor advances in the timing of break-up may have detrimental effects on foraging opportunities, body condition, and subsequent reproduction and survival. The magnitude of seasonal changes in body condition varied across the study area, presumably driven by local environmental conditions. Our results demonstrate how community-based monitoring of polar bears can reveal population-level responses to climate warming in advance of detectable demographic change. Our data on the seasonal timing of polar bear foraging and energy storage should inform predictive models of the effects of climate-mediated sea ice loss.

Seasonal Bioenergetic Changes in Saccostrea glomerata from Two Age Cohorts Farmed in Clyde River, Nsw, Australia

The study measured the mean and ranges of seasonal changes in whole body energetic values in two age groups of the Sydney rock oyster Saccostrea glomerata from the Clyde River, NSW, Australia. Oysters were collected over four seasons from two aquaculture-relevant age groups (24 and 36 mo) identified as key harvesting ages. Protein, lipid, glycogen energy equivalents, and electron transport system (ETS) activity were determined to identify seasonal changes in energy stores and consumption and to calculate cellular energy allocation. There were clear seasonal trends in energy changes, with glycogen and lipid energy equivalents highest in summer, decreasing to their lowest concentrations in autumn, and then slowly increasing through winter and into spring. Protein energy equivalents and ETS activity demonstrated an opposite trend, with increases in autumn and stable through the other seasons. Cellular energy allocation showed seasonal change, with highest values over summer, gradually decreasing in autumn and winter, and then starting to increase again in spring. These results indicate that seasonal changes in temperature, salinity, and food availability as well as reproductive cycles have a significant influence on S. glomerata energy storage and use. Developing an understanding of energetic responses in bivalves in response to environmental conditions can facilitate a more detailed understanding of growth potential and responses to aquaculture practices such as stocking density. As well, understanding natural energetic fluctuations allows a baseline for the assessment of other field-based stress responses such as anthropogenic contamination in S. glomerata.

The association between metabolic profile indices, clinical parameters, and ultrasound measurement of backfat thickness during the periparturient period of dairy cows

This study aimed to evaluate clinical and biochemical changes in dairy cows during periparturient period. It was carried out on 38 multiparous Holstein/Fersian crossbreed dairy cows 3–11 years old. Using ultrasonography for measurement backfat thickness (BFT) for detection of the energy deficit. BFT on dairy cattle is used to monitor changes in subcutaneous fat thickness which represent changes in energy stores. On the basis of clinical examination and assessment of BHBA concentration in blood, cows were classified to four groups, control healthy cows (C = 16), subclinical ketosis (SCK = 10), cows with retained placenta (RP = 6), and clinical mastitis (CM = 6). BFT showed a significant decrease (p < 0.05) after parturition in all diseased groups compared with healthy. The plasma level of NEFA and BHBA showed a significant increase (p < 0.05) at 2 weeks a.p (antepartum) and 2 weeks p.p (postpartum) in RP and SCK than other groups, respectively. The plasma level of glucose showed a significant decrease (p < 0.05) at 2 weeks p.p in SCK group. The plasma level of insulin showed a significant decrease (p < 0.05) at 4 weeks a.p in RP group and in all groups after parturition. It could be concluded that production diseases induced clinical, biochemical, and subcutaneous fat changes in dairy cows.

Modeling energy balance while correcting for measurement error via free knot splines.

Measurements of energy balance components (energy intake, energy expenditure, changes in energy stores) are often plagued with measurement error. Doubly-labeled water can measure energy intake (EI) with negligible error, but is expensive and cumbersome. An alternative approach that is gaining popularity is to use the energy balance principle, by measuring energy expenditure (EE) and change in energy stores (ES) and then back-calculate EI. Gold standard methods for EE and ES exist and are known to give accurate measurements, albeit at a high cost. We propose a joint statistical model to assess the measurement error in cheaper, non-intrusive measures of EE and ES. We let the unknown true EE and ES for individuals be latent variables, and model them using a bivariate distribution. We try both a bivariate Normal as well as a Dirichlet Process Mixture Model, and compare the results via simulation. Our approach, is the first to account for the dependencies that exist in individuals’ daily EE and ES. We employ semiparametric regression with free knot splines for measurements with error, and linear components for error free covariates. We adopt a Bayesian approach to estimation and inference and use Reversible Jump Markov Chain Monte Carlo to generate draws from the posterior distribution. Based on the semiparameteric regression, we develop a calibration equation that adjusts a cheaper, less reliable estimate, closer to the true value. Along with this calibrated value, our method also gives credible intervals to assess uncertainty. A simulation study shows our calibration helps produce a more accurate estimate. Our approach compares favorably in terms of prediction to other commonly used models.

Sugars, Sweet Taste Receptors, and Brain Responses.

Sweet taste receptors are composed of a heterodimer of taste 1 receptor member 2 (T1R2) and taste 1 receptor member 3 (T1R3). Accumulating evidence shows that sweet taste receptors are ubiquitous throughout the body, including in the gastrointestinal tract as well as the hypothalamus. These sweet taste receptors are heavily involved in nutrient sensing, monitoring changes in energy stores, and triggering metabolic and behavioral responses to maintain energy balance. Not surprisingly, these pathways are heavily regulated by external and internal factors. Dysfunction in one or more of these pathways may be important in the pathogenesis of common diseases, such as obesity and type 2 diabetes mellitus.

Effects of Thyroid Hormone Therapy on Cut-Surface Healing of the Remnant Stomach with Short-Term Weight Loss Alterations after Sleeve Gastrectomy

ABSTRACTBackground: The hypothalamic–pituitary–tyhroid axis is directly affected by drastic changes in energy stores. The aim of the present study was to determine the effects of triiodothyronine (T3) treatment on cut-surface healing of remnant stomach with weight loss alterations after sleeve gastrectomy (SG). Methods: Thirty male Wistar Albino rats were divided into three groups: sham (n = 6), control (n = 12), and experimental (n = 12). Control and experimental group rats underwent sleeve gastrectomy. Experimental group rats received a single dose of T3 (400 mg/100 g) on the first postoperative day whereas control group rats received 0.9% NaCl. All rats were sacrificed on the seventh postoperative day. Results: In the group of rats receiving T3, levels of FT3 were significantly higher and that of FT4 were significantly lower compared with both the control and sham group rats (p <.05). No significant difference was found between control and T3 group rats in terms of weight loss (p >.05). Microscopic examination of the cut surface of remnant stomach in the control group rats revealed significantly more severe tissue necrosis, edema, and disruption of mucosal epithelium than in the T3 group rats (p <.05). On the other hand, bridging of the submucosal and muscular layers, tissue granulation, fibroblast accumulation, neoangiogenesis, and collagen deposition in the T3 group rats were significantly higher than in the control group rats (p <.05). Conclusions: Sleeve gastrectomy did not significantly alter thyroid hormone levels in short term. T3 hormone therapy seems to deliver constructive therapeutic effects for wound healing while causing no adverse effect on weight reduction.

Peptides: Basic determinants of reproductive functions

Mammalian reproduction is a costly process in terms of energy consumption. The critical information regarding metabolic status is signaled to the hypothalamus mainly through peripheral peptides from the adipose tissue and gastrointestinal tract. Changes in energy stores produce fluctuations in leptin, insulin, ghrelin and glucose signals that feedback mainly to the hypothalamus to regulate metabolism and fertility. In near future, possible effects of the nutritional status on GnRH regulation can be evaluated by measuring serum or tissue levels of leptin and ghrelin in patiens suffering from infertility. The fact that leptin and ghrelin are antagonistic in their effects on GnRH neurons, their respective agonistic and antagonistic roles make them ideal candidates to use instead of GnRH agonist and antagonist. Similarly, kisspeptin expressing neurons are likely to mediate the well-established link between energy balance and reproductive functions. Exogenous kisspeptin can be used for physiological ovarian hyperstimulation for in-vitro fertilization. Moreover, kisspeptin antagonist therapy can be used for the treatment of postmenapousal women, precocious puberty, PCOS, endometriosis and uterine fibroids. In this review, we will analyze the central mechanisms involved in the integration of metabolic information and their contribution to the control of the reproductive function. Particular attention will be paid to summarize the participation of leptin, kisspeptin, ghrelin, NPY, orexin, urocortin, VIP, insulin, galanin, galanin like peptide, oxytocin, agouti gene-related peptide, and POMC neurons in this process and their possible interactions to contribute to the metabolic control of reproduction.

An objective estimate of energy intake during weight gain using the intake-balance method , ,

Estimates of energy intake (EI) in humans have limited validity. The objective was to test the accuracy and precision of the intake-balance method to estimate EI during weight gain induced by overfeeding. In 2 studies of controlled overfeeding (1 inpatient study and 1 outpatient study), baseline energy requirements were determined by a doubly labeled water study and caloric titration to weight maintenance. Overfeeding was prescribed as 140% of baseline energy requirements for 56 d. Changes in weight, fat mass (FM), and fat-free mass (FFM) were used to estimate change in energy stores (ΔES). Overfeeding EI was estimated as the sum of baseline energy requirements, thermic effect of food, and ΔES. The estimated overfeeding EI was then compared with the actual EI consumed in the metabolic chamber during the last week of overfeeding. In inpatient individuals, calculated EI during overfeeding determined from ΔES in FM and FFM was (mean ± SD) 3461 ± 848 kcal/d, which was not significantly (-29 ± 273 kcal/d or 0.8%; limits of agreement: -564, 505 kcal/d; P = 0.78) different from the actual EI provided (3490 ± 729 kcal/d). Estimated EI determined from ΔES in weight closely estimated actual intake (-7 ± 193 kcal/d or 0.2%; limits of agreement: -386, 370 kcal/d; P = 0.9). In free-living individuals, estimated EI during overfeeding determined from ΔES in FM and FFM was 4123 ± 500 kcal/d and underestimated actual EI (4286 ± 488 kcal/d; -162 ± 301 kcal or 3.8%; limits of agreement: -751, 427 kcal/d; P = 0.003). Estimated EI determined from ΔES in weight also underestimated actual intake (-159 ± 270 kcal/d or 3.7%; limits of agreement: -688, 370 kcal/d; P = 0.001). The intake-balance method can be used to estimate EI during a period of weight gain as a result of 40% overfeeding in individuals who are inpatients or free-living with only a slight underestimate of actual EI by 0.2-3.8%.

Examination of mechanisms (E-MECHANIC) of exercise-induced weight compensation: study protocol for a randomized controlled trial.

BackgroundWeight loss induced only by exercise is frequently less than expected, possibly because of compensatory changes in energy intake and/or energy expenditure. The purpose of the Examination of Mechanisms (E-MECHANIC) of Exercise-Induced Weight Compensation trial is to examine whether increased energy intake and/or reduced spontaneous activity or energy expenditure (outside of structured exercise) account for the less than expected, exercise-associated weight loss.Methods/DesignE-MECHANIC is a three-arm, 6-month randomized (1:1:1) controlled trial. The two intervention arms are exercise doses that reflect current recommendations for (1) general health (8 kcal/kg body weight per week (8 KKW), about 900 kcal/wk) and (2) weight loss (20 KKW, about 2,250 kcal/wk). The third arm, a nonexercise control group, will receive health information only. The sample will include a combined total of 198sedentary, overweight or obese (body mass index: ≥25 kg/m2 to ≤45 kg/m2) men and women ages 18 to 65 years. The exercise dose will be supervised and tightly controlled in an exercise training laboratory. The primary outcome variables are energy intake, which will be measured using doubly labeled water (adjusted for change in energy stores) and laboratory-based food intake tests, and the discrepancy between expected weight loss and observed weight loss. Secondary outcomes include changes in resting metabolic rate (adjusted for change in body mass), activity levels (excluding structured exercise) and body composition. In an effort to guide the development of future interventions, the participants will be behaviorally phenotyped and defined as those who do compensate (that is, fail to lose the amount of weight expected) or do not compensate (that is, lose the amount of weight expected or more).DiscussionIn this study, we will attempt to identify underlying mechanisms to explain why exercise elicits less weight loss than expected. This information will guide the development of interventions to increase exercise-induced weight loss and maximize weight loss retention and related health benefits.Trial registrationClinicalTrials.gov ID: NCT01264406 (registration date: 20 December 2010).

Approaches for quantifying energy intake and %calorie restriction during calorie restriction interventions in humans: the multicenter CALERIE study.

Calorie restriction (CR) is a component of most weight loss interventions and a potential strategy to slow aging. Accurate determination of energy intake and %CR is critical when interpreting the results of CR interventions; this is most accurately achieved using the doubly labeled water method to quantify total energy expenditure (TEE). However, the costs and analytical requirements of this method preclude its repeated use in many clinical trials. Our aims were to determine 1) the optimal TEE assessment time points for quantifying average energy intake and %CR during long-term CR interventions and 2) the optimal approach for quantifying short-term changes in body energy stores to determine energy intake and %CR during 2-wk DLW periods. Adults randomized to a CR intervention in the multicenter CALERIE study underwent measurements of TEE by doubly labeled water and body composition at baseline and months 1, 3, and 6. Average %CR achieved during the intervention was 24.9 ± 8.7%, which was computed using an approach that included four TEE assessment time points (i.e., TEE(baseline, months 1, 3, and 6)) plus the 6-mo change in body composition. Approaches that included fewer TEE assessments yielded %CR values of 23.4 ± 9.0 (TEE(baseline,) months 3 and 6), 25.0 ± 8.7 (TEE(baseline,) months 1 and 6), and 20.9 ± 7.1% (TEE(baseline, month 6)); the latter approach differed significantly from approach 1 (P < 0.001). TEE declined 9.6 ± 9.9% within 2-4 wk of CR beginning and then stabilized. Regression of daily home weights provided the most reliable estimate of short-term change in energy stores. In summary, optimal quantification of energy intake and %CR during weight loss necessitates a TEE measurement within the first month of CR to capture the rapid reduction in TEE.

Self‐Reported, Interview‐Assisted Diet Records Underreport Protein and Energy Intake in Maintenance Hemodialysis (MHD) Patients

Some studies state that MHD patients underreport energy intake (EI) although energy needs are normal and weight is stable over time. Body mass may not reflect changes in energy stores in MHD patients who cannot regulate water balance normally. Validity of dietary data was evaluated by comparing reported EI with actual dietary EI (aEI) in 13 MHD patients participating in a 93‐day N balance study in a research ward to determine protein needs. Resting energy expenditure (REE) was measured prior to admission to estimate total energy expenditure (TEE) and dietary needs to maintain stable weight. Protein intake was changed ~ every 19 days; aEI was constant throughout the study. Total energy requirements were estimated by aEI corrected for changes in body fat measured by DXA over the 93 day study. Underreporting of EI was determined by a EI:REE ratio &lt;1.27 and EI:TEE ratio&lt;1.0.Age was 47.9±9.7 years; BMI, 25.7 ± 4.7 kg/m2. Self‐reported Intake REE (kcals/d ay) TEE (kcals/d ay) EI: RE E EI: TEE kcals/d ay kcals/kg Protei n (g/kg) 1712±4 98 25.4± 7.4 1.03± 0.3 1676±3 31 2134±3 54 1.0 ± 0.2 0.8±0 .2 Body mass and fat were essentially unchanged (−0.87 kg ± 2.02 kg; 0.74 kg ±1.62 kg) during the study suggesting that pre‐study EI was underreported by ~20%. Variance of reported protein and EI was twice that of aEI. Widespread energy underreporting severely compromises the validity of self‐reported, interview‐assisted diet records in MHD patients.

Energy Stores Are Not Altered by Long-Term Partial Sleep Deprivation in Drosophila melanogaster

Recent human studies reveal a widespread association between short sleep and obesity. Two hypotheses, which are not mutually exclusive, might explain this association. First, genetic factors that reduce endogenous sleep times might also impact energy stores, an assertion that we confirmed in a previous study. Second, metabolism may be altered by chronic partial sleep deprivation. Here we address the second assertion by measuring the impact of long-term partial sleep deprivation on energy stores using Drosophila as a model. We subjected flies to long-term partial sleep deprivation via two different methods: a mechanical stimulus and a light stimulus. We then measured whole-body triglycerides and glycogen, two important sources of energy for the fly, and compared them to un-stimulated controls. We also measured changes in energy stores in response to a random circadian clock shift. Sex and line-dependent alterations in glycogen and/or triglyceride levels occurred in response to the circadian clock shift and in flies subjected to a single night of sleep deprivation using light. Thus, consistent with previous studies, our findings suggest that acute sleep loss and changes to the circadian clock can alter metabolism. Significant changes in energy stores were also observed when flies were subjected to chronic sleep loss via the mechanical stimulus, although not the light stimulus. Interestingly, mechanical stimulation resulted in the same change in energy stores even when it was not associated with sleep deprivation, suggesting that the changes are caused by stress rather than sleep loss. These findings emphasize the importance of taking stress into account when evaluating the relationship between sleep loss and metabolism.

Neuroprotective Effect of Long-term MgSO4 Administration After Cerebral Hypoxia-Ischemia in Newborn Rats Is Related to the Severity of Brain Damage

Previous studies have shown contradictory results regarding magnesium-mediated neuroprotection in animal models of perinatal asphyxia. The aim of this study is to investigate the effects of MgSO(4) postasphyxial treatment on hypoxia-ischemia (HI)-induced brain injury in neonatal rats and the possibility that this effect is related to the severity of brain damage. Seven-day-old rats underwent unilateral carotid artery ligation followed by 1 or 2 hours of hypoxia (8% O(2)) and MgSO(4) administration. Adenosine triphosphate/phosphocreatine and glutamate/glutamine measurements and neuropathological evaluation of the hippocampus were used to assess the effects of HI and MgSO(4). HI caused time-dependent changes in energy stores, amino acid concentrations, and brain damage. Administration of MgSO(4) after 1 hour but not after 2 hours of hypoxia resulted in significant prevention of HI-induced brain injury. MgSO(4) administration results in a significant protection against moderate HI-induced brain damage, whereas it fails to offer a similar effect against severe brain damage.

Validation study of energy expenditure and intake during calorie restriction using doubly labeled water and changes in body composition

Background: Clinical trials involving calorie restriction (CR) require an assessment of adherence to a prescribed CR with the use of an objective measure of energy intake (EI).Objective: The objective was to validate the use of energy expenditure (EE) measured by doubly labeled water (DLW), in conjunction with precise measures of body composition, to calculate an individual’s EI during 30% CR.Design: Ten participants underwent 30% CR for 3 wk. During the last week (7 d), 24-h EE was measured in a respiratory chamber and simultaneously by DLW (EEDLW). EI was calculated from 7-d EE measured by DLW and from changes in energy stores (ES) (weight and body composition). Calculated EI was then compared with the actual EI measured in the chamber by using the following equations: calculated EI (kcal/d) = EEDLW + ΔES, where ΔESFM/FFM (kcal/d) = (9.3 × ΔFM, g/d) + (1.1 × ΔFFM, g/d), FM is fat mass, and FFM is fat-free mass.Results: We found close agreement (R = 0.88) between EE measured in the metabolic chamber and EEDLW during CR. Using the measured respiratory quotient, we found that the mean (±SD) EEDLW was 1934 ± 377 kcal/d and EE measured in the metabolic chamber was 1906 ± 327 kcal/d, ie, a 1.3 ± 8.9% overestimation. EI calculated from EEDLW and from changes in ES was 8.7 ± 36.7% higher than the actual EI provided during the chamber stay (1596 ± 656 kcal/d).Conclusions: DLW methods can accurately estimate 24-h EE during CR. Although the mean difference between actual and calculated EIs for the group was small, we conclude that the interindividual variability was too large to provide an assessment of CR adherence on an individual basis.

Effect of age and cold exposure on morphofunctional characteristics of skeletal muscle in neonatal pigs.

Muscular changes accompanying and/or promoting the rapid postnatal improvement of the thermogenic efficiency of shivering were investigated in piglets. Animals were obtained at birth or killed after 5 days at thermoneutrality (34-30 degrees C) or in the cold (24-15 degrees C), to stimulate intense shivering thermogenesis. Fast-twitch-glycolytic (longissimus lumborum) and slow-twitch-oxidative (rhomboid) muscles were prepared for electron microscopic examination and chemical measurements. Muscle-specific changes in energy stores and metabolism were observed after birth, including the switch from glycogen to lipids and variation of the lactate/pyruvate ratio corresponding to the progressive acquisition of the metabolic type of the mature muscles. There was major age-related and/or cold-induced development of the structures involved in excitation-contraction coupling (triadic profiles, +80% in the cold), oxidative metabolism (number of lipid droplets, +81% with age in the cold; number of mitochondria, +29% with age or cold; surface of mitochondrial inner membranes, +18% with age and +32% in the cold) and contraction potential (myofibril volume, +62% with age). In contrast, neither age nor cold affected capillary volume density and capillary-to-fibre ratio. The observed changes reflect the immaturity and remarkable plasticity of piglet skeletal muscle and are likely to underlie its enhanced capacity for shivering thermogenesis after birth.

Energy expenditure in free-living smokers and nonsmokers: comparison between factorial, intake-balance, and doubly labeled water measures

Free-living energy expenditure (EE) was measured in 11 smokers (6 females, 5 males) and 10 nonsmokers (6 females, 4 males) by using three methods. Factorial measures (FEE) used measured basal metabolic rate (BMR), records of time spent in six activity categories over 28 d, and average published energy costs of activities. Intake-balance measures (IBEE) used recorded dietary energy intake and changes in energy stores over 28 d. Doubly labeled water measures (DLWEE) used a two-point method over 8-12 d. Level of activity (1.54 +/- 0.07 and 1.55 +/- 0.06 x BMR) and FEE (9573 +/- 1501 and 9540 +/- 1663 kJ/d) were not different between smokers and nonsmokers, respectively. DLWEE was higher than FEE in both smokers (25.9 +/- 13.5%, P < 0.001) and nonsmokers (10.4 +/- 13.8%, P < 0.05), suggesting factorial underestimation in both groups, although the difference between DLWEE and FEE was significantly greater in smokers than in nonsmokers (P < 0.02). IBEE was higher than FEE in smokers (7.5 +/- 10.1%, P < 0.05) but not different from FEE in nonsmokers (2.7 +/- 16.6%), suggesting factorial underestimation in smokers only. DLWEE was higher than IBEE in smokers (13.8 +/- 12.6%, P < 0.01) but not significantly different from IBEE in nonsmokers (6.2 +/- 16.0%). The discrepancies between DLWEE and IBEE in smokers and DLWEE and FEE in nonsmokers preclude conclusion about absolute levels of daily EE. However, both DLWEE-FEE and IBEE-FEE comparisons suggest that our factorial method underestimates free-living EE in smokers relative to nonsmokers, although the effect is larger with the DLWEE-FEE than with the IBEE-FEE comparison.