Differences In Energy Metabolism Research Articles

Growth retardation at early life and metabolic adaptation among North Korean children.

The high prevalence of obesity is a major public health issue and contributes to the 'double burden' of disease in developing countries. Early exposure to poor nutrition may cause metabolic adaptations that, when accompanied by exposure to 'affluent' nutrition, may increase the risk for obesity and other metabolic disorders. The aim of this study was to determine differences in energy metabolism and nutritional status between normal-height and growth-retarded North Korean children living in South Korea. A total of 29 children were recruited and underwent measurements of resting energy expenditure (REE), respiratory quotient (RQ), anthropometrics and dietary intake. There was no difference in REE or any assessment of obesity between the growth-retarded and normal-height children. Children who were classified as growth retarded (HAZ<-1.0) or stunted (HAZ<-2.0) had a significantly higher RQ (β=0.036 or 0.060, respectively, P=0.018 or 0.016), independent of sex, age, fat-free mass, fat mass and food quotient, compared with children with normal height. The results from this study, the first from an Asian population, add to the growing body of literature suggesting that undernutrition early in life results in adaptations in energy metabolism that favor fat deposition, increasing the risk of stunted children becoming overweight or obese later in life. Continued research on this topic is warranted, given the continued rise in the prevalence of the double burden in transitional countries.

Inhibition of oxidative phosphorylation for enhancing citric acid production by Aspergillus niger.

BackgroundThe spore germination rate and growth characteristics were compared between the citric acid high-yield strain Aspergillus niger CGMCC 5751 and A. niger ATCC 1015 in media containing antimycin A or DNP. We inferred that differences in citric acid yield might be due to differences in energy metabolism between these strains. To explore the impact of energy metabolism on citric acid production, the changes in intracellular ATP, NADH and NADH/NAD+ were measured at various fermentation stages. In addition, the effects of antimycin A or DNP on energy metabolism and citric acid production was investigated by CGMCC 5751.ResultsBy comparing the spore germination rate and the extent of growth on PDA plates containing antimycin A or DNP, CGMCC 5751 was shown to be more sensitive to antimycin A than ATCC 1015. The substrate-level phosphorylation of CGMCC 5751 was greater than that of ATCC 1015 on PDA plates with DNP. DNP at tested concentrations had no apparent effect on the growth of CGMCC 5751. There were no apparent effects on the mycelial morphology, the growth of mycelial pellets or the dry cell mass when 0.2 mg L-1 antimycin A or 0.1 mg L-1 DNP was added to medium at the 24-h time point. The concentrations of intracellular ATP, NADH and NADH/NAD+ of CGMCC 5751 were notably lower than those of ATCC 1015 at several fermentation stages. Moreover, at 96 h of fermentation, the citric acid production of CGMCC 5751 reached up to 151.67 g L-1 and 135.78 g L-1 by adding 0.2 mg L-1 antimycin A or 0.1 mg L-1 DNP, respectively, at the 24-h time point of fermentation. Thus, the citric acid production of CGMCC 5751 was increased by 19.89% and 7.32%, respectively.ConclusionsThe concentrations of intracellular ATP, NADH and NADH/NAD+ of the citric acid high-yield strain CGMCC 5751 were notably lower than those of ATCC 1015. The excessive ATP has a strong inhibitory effect on citric acid accumulation by A. niger. Increasing NADH oxidation and appropriately reducing the concentration of intracellular ATP can accelerate glycolysis and the TCA cycle to enhance citric acid yield.Electronic supplementary materialThe online version of this article (doi:10.1186/s12934-015-0190-z) contains supplementary material, which is available to authorized users.

Mutant TDP-43 deregulates AMPK activation by PP2A in ALS models.

Bioenergetic abnormalities and metabolic dysfunction occur in amyotrophic lateral sclerosis (ALS) patients and genetic mouse models. However, whether metabolic dysfunction occurs early in ALS pathophysiology linked to different ALS genes remains unclear. Here, we investigated AMP-activated protein kinase (AMPK) activation, which is a key enzyme induced by energy depletion and metabolic stress, in neuronal cells and mouse models expressing mutant superoxide dismutase 1 (SOD1) or TAR DNA binding protein 43 (TDP-43) linked to ALS. AMPK phosphorylation was sharply increased in spinal cords of transgenic SOD1G93A mice at disease onset and accumulated in cytoplasmic granules in motor neurons, but not in presymptomatic mice. AMPK phosphorylation also occurred in peripheral tissues, liver and kidney, in SOD1G93A mice at disease onset, demonstrating that AMPK activation occurs late and is not restricted to motor neurons. Conversely, AMPK activity was drastically diminished in spinal cords and brains of presymptomatic and symptomatic transgenic TDP-43A315T mice and motor neuronal cells expressing different TDP-43 mutants. We show that mutant TDP-43 induction of the AMPK phosphatase, protein phosphatase 2A (PP2A), is associated with AMPK inactivation in these ALS models. Furthermore, PP2A inhibition by okadaic acid reversed AMPK inactivation by mutant TDP-43 in neuronal cells. Our results suggest that mutant SOD1 and TDP-43 exert contrasting effects on AMPK activation which may reflect key differences in energy metabolism and neurodegeneration in spinal cords of SOD1G93A and TDP-43A315T mice. While AMPK activation in motor neurons correlates with progression in mutant SOD1-mediated disease, AMPK inactivation mediated by PP2A is associated with mutant TDP-43-linked ALS.

Mutant TDP-43 Deregulates AMPK Activation by PP2A in ALS Models

Bioenergetic abnormalities and metabolic dysfunction occur in amyotrophic lateral sclerosis (ALS) patients and genetic mouse models. However, whether metabolic dysfunction occurs early in ALS pathophysiology linked to different ALS genes remains unclear. Here, we investigated AMP-activated protein kinase (AMPK) activation, which is a key enzyme induced by energy depletion and metabolic stress, in neuronal cells and mouse models expressing mutant superoxide dismutase 1 (SOD1) or TAR DNA binding protein 43 (TDP-43) linked to ALS. AMPK phosphorylation was sharply increased in spinal cords of transgenic SOD1G93A mice at disease onset and accumulated in cytoplasmic granules in motor neurons, but not in pre-symptomatic mice. AMPK phosphorylation also occurred in peripheral tissues, liver and kidney, in SOD1G93A mice at disease onset, demonstrating that AMPK activation occurs late and is not restricted to motor neurons. Conversely, AMPK activity was drastically diminished in spinal cords and brains of presymptomatic and symptomatic transgenic TDP-43A315T mice and motor neuronal cells expressing different TDP-43 mutants. We show that mutant TDP-43 induction of the AMPK phosphatase, protein phosphatase 2A (PP2A), is associated with AMPK inactivation in these ALS models. Furthermore, PP2A inhibition by okadaic acid reversed AMPK inactivation by mutant TDP-43 in neuronal cells. Our results suggest that mutant SOD1 and TDP-43 exert contrasting effects on AMPK activation which may reflect key differences in energy metabolism and neurodegeneration in spinal cords of SOD1G93A and TDP-43A315T mice. While AMPK activation in motor neurons correlates with progression in mutant SOD1-mediated disease, AMPK inactivation mediated by PP2A is associated with mutant TDP-43-linked ALS.

Enhanced detection of metastatic prostate cancer cells in human plasma with lipid bodies staining

BackgroundReprogramming of energy metabolism of malignant cancer cells confers competitive advantage in growth environments with limited resources. However, not every process of cancer development is associated with competition for resources. During hematogenous transport, cancer cells are exposed to high levels of oxygen and nutrients. Does energy metabolism of cancer cells change as a function of exposure to the bloodstream? Could such changes be exploited to improve the detection of circulating tumor cells (CTC)? These questions have clinical significance, but have not yet been sufficiently examined.MethodsThe energy metabolism was examined as a function of incubation in nutrient-rich plasma in prostate metastatic cancer cells LNCaP and non-transformed prostate epithelial cells RWPE1. Uptake kinetics of a fluorescent glucose analog (2-NBD) and lipophilic dyes (DiD & Bodipy) were measured in both cell lines, as well as in peripheral blood mononuclear cells (PBMC).ResultsLNCaP cells exhibited hyper-acetylation of low molecular weight proteins compared to RWPE1 cells. Following plasma incubation, protein lysine acetylation profile was unchanged for LNCaP cells while significantly altered for RWPE1 cells. O-linked glycosylated protein profiles were different between LNCaP and RWPE1 cells and varied in both cell lines with plasma incubation. Maximal respiration or glycolytic capacities was unchanged in LNCaP cells and impaired in RWPE1 cells following plasma incubation. However, the uptake rates of 2-NBD and DiD were insufficient for discrimination of LNCaP, or RWPE1 cells from PBMC. On the other hand, both RWPE1 and LNCaP cells exhibited intracellular lipid bodies following plasma incubation; whereas, PBMC did not. The presence of lipid bodies in LNCaP cells permitted retention of Bodipy dye and allowed discrimination of LNCaP cells from PBMC with flow cytometry.ConclusionsDespite clear differences in energy metabolism, metastatic prostate cancer cells could not be efficiently distinguished from non-transformed prostate epithelial cells using fluorescent glucose or lipid uptake kinetics. However, metastatic prostate cancer cells in plasma could be clearly distinguished from blood nucleated cells due to the presence of intracellular lipid bodies. Fluorescent labeling of lipid bodies permitted a simple and sensitive means for high throughput detection of metastatic prostate cancer cells in human plasma.

Gender-specific differences in energy metabolism during the initial phase of critical illness

Women and men differ in substrate and energy metabolism. Such differences may affect energy requirements during the acute phase of critical illness. Data of 155 critically ill medical patients were reviewed for this study. Indirect calorimetry in each patient was performed within the first 72 h following admission to the medical intensive care unit after an overnight fast. In overweight (body mass index (BMI) ≥25 kg/m(2)) but not in normal-weight patients, resting energy expenditure (REE) adjusted for body weight (REEaBW) differed significantly between women and men (17.2 (interquartile range (IQR) 15.2-20.7) vs 20.9 (IQR 17.9-23.4) kcal/kg/day, P<0.01). Similarly, REE adjusted for ideal body weight (REEaIBW) was significantly lower in women compared with men (25.5 (IQR 22.6-28.1) vs 28.0 (IQR 25.2-30.0) kcal/kg/day, P<0.05). In overweight patients, gender was identified as an independent predictor of REEaBW in the multivariate regression model (r=-2.57 (95% CI -4.57 to -0.57); P<0.05), even after adjustment for age, simplified acute physiology score (SAPS II), body temperature, body weight and height. REEaBW decreases with increasing body mass in both sexes. This relationship differs between women and men. Overweight critically ill women show significantly lower REEaBW and REEaIBW, respectively, compared with men. These findings could affect the current practice of nutritional support during the early phase of critical illness.

Metabolism targeting therapy of dichloroacetate-loaded electrospun mats on colorectal cancer

Differences in energy metabolism between tumor cells and normal cells offer an attractive avenue of research into drug targets for tumor therapy. The use of a metabolic modulator (sodium dichloroacetate, DCA), administered in situ, to reverse the “Warburg effect” of tumor cells has been demonstrated as an effective tumor therapy. Herein, DCA and diisopropylamine dichloroacetate (DADA) were incorporated separately into polylactide (PLA) electrospun mats and applied to C26 tumor-bearing mice via in situ administration. After 12 d of treatment, the tumor suppression rates of 75% and 84% were achieved in the DC group (treated with a DCA-loaded mat) and the DA group (treated with a DADA-loaded mat), respectively. With tolerable physiologic toxicity under high local concentration, the DA group showed a 95% tumor suppression rate without any recurrence after 15 d of therapy. The desirable therapeutic effects of these metabolic modulators should ascribe to the energy-central metabolism-targeting effects of DCA and DADA, which were demonstrated both in vitro and in vivo. Therefore, DCA- and DADA-loaded mats are the effective anti-cancer drugs dosages to discriminate between tumor cells and normal cells for minimizing systemic toxicity.

Bone quality and strength are greater in growing male rats fed fructose compared with glucose

Optimization of peak bone mass during adolescence is important for osteoporosis prevention. Studies in rodents and humans have demonstrated the harmful effects of sugar intake on bone health. With the high levels of sucrose in the diets of adolescents, it is necessary to understand the influence of glucose and fructose on growing bones. This study compared the effects of dietary glucose and fructose on bone formation, microarchitecture, and strength. Because of the different metabolic effects of glucose and fructose, we hypothesized that their individual effects on bone would be different. Eighteen male Sprague-Dawley rats (age, 60 days) were randomly assigned to high-fructose (n = 9; 40% fructose, 10% glucose) or high-glucose diet (n = 9; 50% glucose) for 12 weeks. Bone measurements included histology and histomorphometry of trabecular bone in the distal femur and a 3-point bending test of the whole tibia. Whole liver mass and postprandial serum glucose, insulin, and triglycerides were used to assess differences in energy metabolism between the diets. There were no differences in food intake, body weight, or visceral adiposity between groups, but fructose consumption led to heavier livers (P = .001) and elevated serum triglycerides (P = .00). The distal femurs of fructose-fed rats had greater bone volume (bone volume/total volume; P = .03), lower bone surface (bone surface/bone volume; P = .02), and thicker trabeculae (trabecular thickness; P = .01). The tibias of the fructose-fed rats also withstood a greater maximum flexure load (P = .032). These results indicate that consumption of the high-fructose diet resulted in stronger bones with enhanced microarchitecture than consumption of the high-glucose diet.

Recovery pattern of non-protein respiratory quotient and non-esterified fatty acids after liver resection

ObjectivePerioperative nutritional care is important to maintain preoperative and postoperative nutritional status. However, few reports have investigated energy metabolism after hepatectomy. The aim of this study was to determine differences in energy metabolism, blood biochemistry, and nutritional status before and after liver resection in patients with hepatocellular carcinoma (HCC) and healthy living donors for liver transplantation. MethodsEighteen hospitalized patients with HCC group and 13 living donors for liver transplantation (donor group) were enrolled in this study. The donor group was divided into two groups on the basis of age; Y-donor group (age < 40 y, n = 7), and O-donor group (age ≥ 40 y, n = 6). Energy metabolism was measured by indirect calorimetry at preoperative day and postoperative day (POD) 7 and 14, and blood biochemistry was also examined. ResultsRecovery of non-protein respiratory quotient (npRQ) and blood biochemical data such as total bilirubin, aspartate aminotransferase and alanine aminotransferase levels were observed in Y-donor group on POD 14. However, although biochemical data improved in the HCC and O-donor group, npRQ remained unchanged on POD 14. ConclusionsImprovement of npRQ took longer than blood biochemical data in patients with HCC and older donors. Because the recovery of npRQ is associated with donor age, careful nutritional management may be required for a longer time depending on the pathophysiological condition of each patient after hepatectomy.

Metabolic profiles of ketolysis and glycolysis in malignant gliomas: Possible predictors of response to ketogenic diet therapy.

e13048 Background: The enzymatic differences in energy metabolism between normal brain tissues and malignant gliomas formed the basis for animal model studies that showed increased survival in mice with orthotopically transplanted glioblastoma multiforme (GBM) treated with energy restricted ketogenic diet (ERKD). To test the hypothesis that human brain tumors may also be sensitive to ERKD, we used immunohistochemistry reactions on formalin fixed paraffin embedded tumor samples to evaluate for the presence of enzymes important for the metabolism of ketones and glucose. Methods: Immunoreactivities were graded using a semi-quantitative scale based on the percentage of positive cells: low positive&lt;5% (LOW); intermediate (INT) 5-20%; and highly positive (HIGH) &gt;20%. Focal non-neoplastic “normal” brain tissue present within the specimens served as positive internal controls. Results: Succinyl CoA: 3-oxoacid CoA transferase (OXCT1) and 3-hydroxybutyrate dehydrogenase 1 (BDH1) are mitochondrial enzymes important for metabolizing beta hydroxy butyrate, the main ketone in blood. Both of these enzymes were either decreased or absent (INT or LOW) concordantly in 14 of the 17 (82%) GBMs, and in 1 of 6 (17%) anaplastic astrocytomas (AA). Two of the enzymes in the glycolytic pathway hexokinase-2 and pyruvate kinase M2 were concordantly LOW or INT in only 3 of the 17 GBMs that also were LOW or INT for both OXCT1 and BDH1. The remaining brain tumors were positive for at least one of these glycolytic enzymes. Mitochondrial enzymes were not globally deficient. The mitochondrial enzyme acetyl CoA transferase (ACAT1) was present in 9 of the 14 GBM specimens that were LOW or INT for the mitochondrial enzymes OXCT1 and BDH1. Conclusions: Our data showing that many, but not all, malignant gliomas lack ketolytic enzymes, support the rationale of ERKD as investigational treatment for patients with malignant gliomas. Moreover, we hypothesize that it is important to test individual tumor samples for the expression of these enzymes prior to ERKD, as patients with malignant gliomas that have diminished capacity to metabolize ketones likely may derive the most benefit from ERKD.

Microbial Oncotarget: Bacterial-Produced Butyrate, Chemoprevention and Warburg Effect

Microbial Oncotarget: Bacterial-Produced Butyrate, Chemoprevention and Warburg Effect

NAD+ and Nicotinamide: Sex Differences in Cerebral Ischemia

BackgroundPrevious literature suggests that cell death pathways activated after cerebral ischemia differ between the sexes. While caspase-dependent mechanisms predominate in the female brain, caspase-independent cell death induced by the activation of poly(ADP-ribose) polymerase (PARP) predominates in the male brain. PARP-1 gene deletion decreases infarction volume in the male brain, but paradoxically increases damage in PARP-1 knockout females. PurposeThis study examined stroke-induced changes in NAD+, a key energy molecule involved in PARP-1 activation in both sexes. MethodsMice were subjected to middle cerebral artery occlusion and NAD+ levels were assessed. Caspase-3 activity and nuclear translocation were assessed 6h after ischemia. In additional cohorts, Nicotinamide (500mg/kg i.p.) a precursor of NAD+ or vehicle was administered and infarction volume was measured 24h after ischemia. ResultsMales have higher baseline NAD+ levels than females. Significant stroke-induced NAD+ depletion occurred in males and ovariectomized females but not in intact females. PARP-1 deletion prevented the stroke-induced loss in NAD+ in males, but worsened NAD+ loss in PARP-1 deficient females. Preventing NAD+ loss with nicotinamide reduced infarct in wild-type males and PARP-1 knockout mice of both sexes, with no effect in WT females. Caspase-3 activity was significantly increased in PARP-1 knockout females compared to males and wild-type females, this was reversed with nicotinamide. ConclusionsSex differences exist in baseline and stroke-induced NAD+ levels. Nicotinamide protected males and PARP knockout mice, but had minimal effects in the wild-type female brain. This may be secondary to differences in energy metabolism between the sexes.

Photosynthetic acclimation responses of maize seedlings grown under artificial laboratory light gradients mimicking natural canopy conditions

In this study we assessed the ability of the C4 plant maize to perform long-term photosynthetic acclimation in an artificial light quality system previously used for analyzing short-term and long-term acclimation responses (LTR) in C3 plants. We aimed to test if this light system could be used as a tool for analyzing redox-regulated acclimation processes in maize seedlings. Photosynthetic parameters obtained from maize samples harvested in the field were used as control. The results indicated that field grown maize performed a pronounced LTR with significant differences between the top and the bottom levels of the plant stand corresponding to the strong light gradients occurring in it. We compared these data to results obtained from maize seedlings grown under artificial light sources preferentially exciting either photosystem II or photosystem I. In C3 plants, this light system induces redox signals within the photosynthetic electron transport chain which trigger state transitions and differential phosphorylation of LHCII (light harvesting complexes of photosystem II). The LTR to these redox signals induces changes in the accumulation of plastid psaA transcripts, in chlorophyll (Chl) fluorescence values F\\rm s/F\\rm m, in Chl a/b ratios and in transient starch accumulation in C3 plants. Maize seedlings grown in this light system exhibited a pronounced ability to perform both short-term and long-term acclimation at the level of psaA transcripts, Chl fluorescence values F\\rm s/F\\rm m and Chl a/b ratios. Interestingly, maize seedlings did not exhibit redox-controlled variations of starch accumulation probably because of its specific differences in energy metabolism. In summary, the artificial laboratory light system was found to be well-suited to mimic field light conditions and provides a physiological tool for studying the molecular regulation of the LTR of maize in more detail.

Low concentrations of Rhodamine-6G selectively destroy tumor cells and improve survival of melanoma transplanted mice

Rhodamine-6G is a fluorescent dye binding to mitochondria, thus reducing the intact mitochondria number and inhibiting mitochondrial metabolic activity. Resultantly, the respiratory chain functioning becomes blocked, the cell "suffocated" and eventually destroyed. Unlike normal cells, malignant cells demonstrate a priori reduced mitochondrial numbers and aberrant metabolism. Therefore, a turning point might exist, when Rhodamine-induced loss of active mitochondria would selectively destroy malignant, but spare normal cells. Various malignant vs. non-malignant cell lines were cultured with Rhodamine-6G at different concentrations. In addition, C57Bl mice were implanted with B16-F10 melanoma and treated with Rhodamine-6G at different dosage/time regimens. Viability and proliferation of cultured tumor cells were time and dose-dependently inhibited, up to 90%, by Rhodamine-6G, with profound histological signs of cell death. By contrast, inhibition of normal control cell proliferation hardly exceeded 15-17%. Melanoma-transplanted mice receiving Rhodamine-6G demonstrated prolonged survival, improved clinical parameters, inhibited tumor growth and metastases count, compared to their untreated counterparts. Twice-a-week 10-6M Rhodamine-6G regimen yielded the most prominent results. We conclude that malignant, but not normal, cells are selectively destroyed by low doses of Rhodamine-6G. In vivo, such treatment selectively suppresses tumor progression and dissemination, thus improving prognosis. We suggest that selective anti-tumor properties of Rhodamine-6G are based on unique physiologic differences in energy metabolism between malignant and normal cells. If found clinically relevant, low concentrations of Rhodamine-6G might be useful for replacing, or backing up, more aggressive nonselective chemotherapeutic compounds.

Metabolite changes in the greasy tongue coating of patients with chronic gastritis

To explore the changes in metabolites in the greasy tongue coating in patients with chronic gastritis. Forty chronic gastritis patients presenting with greasy tongue coating, 30 chronic gastritis patients presenting with non-greasy tongue coating, and 20 healthy control persons presenting with light red tongues and thin white coating were enrolled, and the tongue coating was detected by combining artificial diagnosis and the Z-BOX Tongue Digital Analyzer's diagnosis. Samples of all the tongue coatings were collected before treatment. The metabolic fingerprinting of the tongue coating samples was obtained using ultra-performance liquid chromatography and mass spectrometry (UPLC-MS), and the metabolic components in the tongue coating samples were detected. After this, principal component analysis, partial least squares discriminant analysis and orthogonal partial least squares discriminant analysis (OPLS-DA) were used to identify potential metabolic markers. Finally, the components were identified using the Chemspider and HMDB searching. UPLC-MS results were analyzed by OPLS-DA and showed that the metabolites among the three groups were distributed in different regions. The different potential metabolic markers between the patients with or without greasy coating were 3-ketolactose, 2-deoxy-D-ribose, UDP-D-galactose metarhodopsin, ascorbate, picolinate and histidine. The different potential metabolic markers between the greasy coating group and the normal group were 3-ketolactose, UDP-D-galactose, leukotriene A4 and vitamin D(2). The metabolites of the greasy coating group, the non-greasy coating group and the normal group show significant differences in energy metabolism, mainly of glucose metabolism. This demonstrated that glucose metabolism may be one of the mechanisms leading to the formation of greasy coating.

Yeast respiration of sugars by non-Saccharomyces yeast species: A promising and barely explored approach to lowering alcohol content of wines

The increasing ethanol content is a major challenge imposed by climate change on the production of quality wines. We propose a strategy for lowering ethanol production during grape must fermentation by taking advantage of the differences in energy metabolism among ascomycetous wine yeast species. We hypothesize that using carefully selected yeast strains the available oxygen would be taken up by yeast cells for the respiration of a significant fraction of the hexoses present in grape must. The actual degree of sugar consumption by this pathway, and the concomitant reduction in the final ethanol yield, would depend among other factors on the amount of available oxygen, in turn depending on standard winemaking practices or ad hoc aeration regimes. Setting up this strategy would involve the birth of a new research field, integrating topics like quantitative analysis of the energy and overall metabolism of non-Saccharomyces yeast species under winemaking conditions, interactions between yeast strains of different species in the grape must environment, or the impact of eventual ad hoc oxygenation treatments on must and wine constituents.

Energy requirement for maintenance and efficiency of energy utilization for growth in juvenile turbot (Psetta maxima, L.): The effect of strain and replacement of dietary fish meal by wheat gluten

Restricted ration level experiments were realized to determine the gross, digestible and metabilizable energy requirements for maintenance (GEm; DEm; MEm) and the efficiencies of energy utilization for growth (kg(GE); kg(DE); kg(ME)) in juvenile turbot. The effects of the fish strain (Denmark, DK; Iceland, IS) as well as the partial replacement of fish meal by wheat gluten in the diet were examined as possible factors affecting the energy metabolism. Turbot (initial body weight 49g) were reared in a recirculation aquaculture system supplied with seawater at a temperature of 17±0.6°C and 26±1.2ppt salinity for 67days. Two diets, differing in wheat gluten content (80g or 330gkg−1 diet) were fed at six increasing feeding levels, from near maintenance to ad libitum levels, once a day per hand. Chemical composition and energy content of body weight gain were determined by using the comparative slaughter technique. Linear regression analyses were applied to obtain GEm, DEm, MEm, kg(GE), kg(DE) and kg(ME).GEm, DEm and MEm were 21.6–29.8, 17.0–23.5 and 15.5–21.4kJkg−0.8d−1, respectively, and kg(GE), kg(DE) and kg(ME) were 0.46–0.49, 0.59–0.64 and 0.63–0.68, respectively. Values for GEm, DEm and MEm as well as for kg(GE), kg(DE) and kg(ME) in turbot from IS were significantly higher than in fish from DK, but without any effect on energy retention at high feeding levels. Turbot receiving the diet where fish meal was partially replaced by wheat gluten showed higher GEm, DEm and MEm as well. No effect on energy retention at high feeding levels was observed again. It is concluded that differences in energy metabolism between strains might be considered when selecting turbot for aquaculture production.

Comparison of blood variables, fiber intensity, and muscle metabolites in hot-boned muscles from electrical- and gas-stunned broilers

The aim of this study was to compare the effects of gas stunning (GS) and electrical stunning (ES) on energy metabolism in Arbor Acres broilers. Thirty-six birds were slaughtered without stunning (control) or after stunning with the following treatments: 40% CO(2) + 21% O(2) + N(2) (G40%); 60% CO(2) + 21% O(2) + N(2) (G60%); 35 V, 47 mA, 400 Hz (E35V); 50 V, 67 mA, 160 Hz (E50V); and 65 V, 86 mA, 1,000 Hz (E65V). Muscle samples were obtained from the pectoralis major (breast) and tibialis anterior (leg) muscles in ambient temperature within 45 min postmortem and stored at -80°C. Blood pH decreased consistently with GS (G40% and G60%) compared with ES and the control (P < 0.01). No consistent differences were observed between GS and ES in the plasma variables, glycolytic potential, adenosine phosphates, or fiber intensities. Plasma lactate increased with G40% and E35V (P < 0.05), whereas plasma uric acid and urea nitrogen increased with E35V (P < 0.05) compared with the control. Compared with the control, the intensity of type IIB fibers decreased in broilers stunned with E35V and E50V (P < 0.05) and glycolytic potential increased (P < 0.01) with G60% in the breast muscle and decreased (P < 0.01) in the leg muscle with all the stunning treatments except for E50V. Energy decreased (lower adenosine triphosphate, higher adenosine monophosphate, and adenosine monophosphate:adenosine triphosphate ratio, P < 0.05) in breast muscle with G40% compared with ES at high currents (E50V and E65V). However, the adenosine phosphates with GS were not significantly different (P > 0.05) from ES at low current (E35V) in either breast or leg muscle. In conclusion, no essential difference in energy metabolism was found in broilers stunned with ES and GS when ES was based on low current and high frequency and GS was based on hypercapnic moderate oxygenation. This study indicated that G40% was potentially a superior stunning variable.

Sex differences in energy metabolism in pre-pubescent, early pubescent and adult rats

This study was intended to investigate sex differences in response to a high fat (HF) diet at three stages, pre-puberty, early puberty, and adulthood. Body weight, energy intake, glucose, insulin, and leptin concentrations were measured in male and female rats that were fed either a HF or a control chow during each stage of development. The sex hormones of adult rats were also examined. In addition, metabolic factors of male rats pair-fed with females were evaluated. At pre-puberty, the average body weight of pups born to a HF dam exceeded that of the control, whereas there were no significant differences in body weight between males and females. During early puberty and among 15-wk-old rats, males exhibited greater weight gain with higher energy intake than did females. During all three stages, HF rats exhibited significant increases in body weight, insulin and leptin concentrations. Estradiol levels of females were higher than those of males, and those of the HF groups were significantly lower than the control groups. Although the body weight gain in male rats pair-fed with females exceeded that of the females, the insulin and leptin levels of pair-fed HF males decreased to the control levels. HF male rats became obese earlier than HF females. This result may be the result of differences in estradiol levels between males and females. The decline of insulin and leptin levels in pair-fed male groups indicates that caloric restriction among male rats could reduce the incidence of metabolic diseases.

Sex Differences in Energy Metabolism Need to Be Considered with Lifestyle Modifications in Humans

Women have a higher proportion of body fat compared to men. However, women consume fewer kilojoules per kilogram lean mass and burn fat more preferentially during exercise compared with men. During gestation, women store even greater amounts of fat that cannot be solely attributed to increased energy intake. These observations suggest that the relationship between kilojoules consumed and kilojoules utilised is different in men and women. The reason for these sex differences in energy metabolism is not known; however, it may relate to sex steroids, differences in insulin resistance, or metabolic effects of other hormones such as leptin. When considering lifestyle modifications, sex differences in energy metabolism should be considered. Moreover, elucidating the regulatory role of hormones in energy homeostasis is important for understanding the pathogenesis of obesity and perhaps in the future may lead to ways to reduce body fat with less energy restriction.