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This study investigated whether carbohydrate-energy replacement immediately after prolonged endurance exercise attenuates insulin sensitivity the following morning, and whether exercise improves insulin sensitivity the following morning independent of an exercise-induced carbohydrate deficit. Oral glucose tolerance and whole-body insulin sensitivity were compared the morning after 3 evening conditions, involving (1) treadmill exercise followed by a carbohydrate replacement drink (200 or 150 g maltodextrin for males and females, respectively; CHO-replace); (2) treadmill exercise followed by a non-caloric, taste-matched placebo (CHO-deficit); or (3) seated rest with no drink provided (Rest). Treadmill exercise involved 90 minutes at ∼80% age-predicted maximum heart rate. Seven males and 2 females (aged 23 ± 1 years; body mass index 24.0 ± 2.7 kg·m−2) completed all conditions in a randomised order. Matsuda index improved by 22% (2.2 [0.3, 4.0] au, p = 0.03) and HOMA2-IR improved by 10% (–0.04 [–0.08, 0.00] au, p = 0.04) in CHO-deficit versus CHO-replace, without corresponding changes in postprandial glycaemia. Outcomes were similar between Rest and other conditions. These data suggest that improvements to insulin sensitivity in healthy populations following acute moderate/vigorous intensity endurance exercise may be dependent on the presence of a carbohydrate-energy deficit. Novelty: Restoration of carbohydrate balance following acute endurance exercise attenuated whole-body insulin sensitivity. Exercise per se failed to enhance whole-body insulin sensitivity. Maximising or prolonging the post-exercise carbohydrate deficit may enhance acute benefits to insulin sensitivity. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Animal Science is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Canadian Journal of Animal Science is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The present study aimed to compare the early metabolic response between high-load resistance exercise (HL-RE) and low-load resistance exercise with blood flow restriction (LL-BFR). Nine young, well-trained men participated in a randomized crossover design in which each subject completed LL-BFR, HL-RE, or condition control (no exercise) with a 1-week interval between them. Blood samples were taken immediately before and 5 min after the exercise sessions. Nuclear magnetic resonance spectroscopy identified and quantified 48 metabolites, 6 of which presented significant changes among the exercise protocols. The HL-RE promoted a higher increase in pyruvate, lactate, and alanine compared with the LL-BFR and the control. HL-RE and LL-BFR promoted a higher increase in succinate compared with the control; however, there was no difference between HL-RE and LL-BFR. Also, while there was no difference in acetoacetate between HL-RE and LL-BFR, a greater decrease was observed in both compared with the control. Finally, LL-BFR promoted a greater decrease in choline compared with the control. In conclusion, this study provides by metabolomics a new insight in metabolic response between LL-BFR and HL-RE by demonstrating a distinct response to some metabolites that are not commonly analyzed. [ABSTRACT FROM AUTHOR]

We discuss the origin of 4-aminobutyrate (GABA) from glutamate and polyamines, and its subsequent catabolism to succinic semialdehyde and either succinate or 4-hydroxybutyrate. Promiscuous activities of GABA transaminase, glyoxylate/succinic semialdehyde reductases, and aldehyde dehydrogenase 10As appear to be important determinants of cross-talk among metabolic pathways during stress. Imposition of abiotic stress, as well as genetic or chemical disruption of glutamate decarboxylase, GABA transaminase, and tricarboxylic acid cycle reactions, results in non-cyclic carbon flux in the tricarboxylic acid cycle, demonstrating that stress-induced GABA metabolism is strongly linked with respiration. Metabolic generation of 4-hydroxybutyrate is probably linked to the stimulation of succinic semialdehyde reductase activity by an increasing NADPH/NADP+ ratio. We discuss the potential signaling role of GABA in various processes, including pollen tube guidance, interaction with fungal, bacterial, and invertebrate pests, and stomatal functioning, and argue that further research on short-term responses to stress is required to determine whether or not GABA functions by binding to or regulating the activity of GABA receptor molecules. Finally, we describe how emerging information about the metabolic and signaling roles of GABA is being used to improve plant defenses against biotic and abiotic stresses, and benefit human health. [ABSTRACT FROM AUTHOR]

Although it is known that altitude impairs performance in endurance sports, there is no consensus on the involvement of energy substrates in this process. The objective of the present study was to determine whether the metabolomic pathways used during endurance exercise differ according to whether the effort is performed at sea level or at moderate altitude (at the same exercise intensity, using proton nuclear magnetic resonance, 1H NMR). Twenty subjects performed two 60-min endurance exercise tests at sea level and at 2150 m at identical relative intensity on a cycle ergometer. Blood plasma was obtained from venous blood samples drawn before and after exercise. 1H NMR spectral analysis was then performed on the plasma samples. A multivariate statistical technique was applied to the NMR data. The respective relative intensities of the sea level and altitude endurance tests were essentially the same when expressed as a percentage of the maximal oxygen uptake measured during the corresponding incremental maximal exercise test. Lipid use was similar at sea level and at altitude. In the plasma, levels of glucose, glutamine, alanine, and branched-chain amino acids had decreased after exercise at altitude but not after exercise at sea level. The decrease in plasma glucose and free amino acid levels observed after exercise at altitude indicated that increased involvement of the protein pathway was necessary but not sufficient for the maintenance of glycaemia. Metabolomics is a powerful means of gaining insight into the metabolic changes induced by exercise at altitude. [ABSTRACT FROM AUTHOR]

Over the last 2 decades, mi(cro)RNAs have emerged as one of the key regulators of metabolic homeostasis. Most of the studies have highlighted that, in the cytoplasm, miRNAs directly bind to the 3′-UTR (untranslated region) of a mRNA. Conventional RNA-induced silencing complex (RISC) formation results in the post-transcriptional inhibition. This process is known to contribute to the development of metabolic diseases, including diabetes mellitus. Recent advancements with small RNA detection technologies have enabled us to identify miRNAs in the mitochondrial compartment of the cells. We have termed these miRNAs, which translocate into the mitochondria as mitochondrial miRNA, MitomiR. It has been demonstrated that MitomiRs can regulate gene expression, with some evidence even suggesting that, after translocation, MitomiRs can bind to the 3′-end of a mitochondrial gene, altering its regulation. Our main focus in this review is to highlight the potential role of MitomiR in the pathogenesis of metabolic disorders such as diabetes mellitus. [ABSTRACT FROM AUTHOR]

Raloxifene (RLX) is a selective estrogen receptor modulator widely used for the treatment of osteoporosis in post-menopause women. Toxicological in vitro studies suggested the reactivity of RLX through phase I metabolism. Herein, we describe a simple and inexpensive method for monitoring the reactive metabolism and detoxification of RLX by electrochemistry (EC) and mass spectrometry (MS). The phase I metabolite was synthesized electrochemically on a screen-printed electrode (SPE) and subsequently reacted with glutathione (GSH). The resulted GSH-adducts and GSH disulfides were characterized off-line by electrospray ionization (ESI)-MS. [ABSTRACT FROM AUTHOR]

This study investigated the impact of raising plasma beta-hydroxybutyrate (β-OHB) through ingestion of ketone salts on substrate oxidation and performance during cycling exercise. Ten healthy adult males (age, 23 ± 3 years; body mass index, 25 ± 3 kg/m2, peak oxygen uptake, 45 ± 10 mL/(kg·min)−1) were recruited to complete 2 experimental trials. Before enrollment in the experimental conditions, baseline anthropometrics and cardiorespiratory fitness (peak oxygen uptake) were assessed and familiarization to the study protocol was provided. On experimental days, participants reported to the laboratory in the fasted state and consumed either 0.3 g/kg β-OHB ketone salts or a flavour-matched placebo at 30 min prior to engaging in cycling exercise. Subjects completed steady-state exercise at 30%, 60%, and 90% ventilatory threshold (VT) followed by a 150-kJ cycling time-trial. Respiratory exchange ratio (RER) and total substrate oxidation were derived from indirect calorimetry. Plasma glucose, lactate, and ketones were measured at baseline, 30 min post-supplement, post-steady-state exercise, and immediately following the time-trial. Plasma β-OHB was elevated from baseline and throughout the entire protocol in the ketone condition ( p < 0.05). RER was lower at 30% and 60% VT in the ketone compared with control condition. Total fat oxidation was greater in the ketone versus control ( p = 0.05). Average time-trial power output was ∼7% lower (-16 W, p = 0.029) in the ketone condition. Ingestion of ketone salts prior to exercise increases fat oxidation during steady-state exercise but impairs high-intensity exercise performance. [ABSTRACT FROM AUTHOR]

This study examined the metabolic response of lung cancer cells and normal lung fibroblasts to hypoxia and acidity. GLUT1 and HXKII mRNA/protein expression was up-regulated under hypoxia in the MRC5 fibroblasts and in the A549 and H1299 lung cancer cell lines, indicating intensified glucose absorption and glycolysis. Under hypoxia, the LDHA mRNA and LDH5 protein levels increased in the cancer cells but not in the fibroblasts. Acidity suppressed the above-mentioned hypoxia effect. PDH-kinase-1 (PDK1 mRNA and protein) and inactive phosphorylated-PDH protein levels were induced under hypoxia in the cancer cells, whereas these were reduced in the MRC5 lung fibroblasts. In human tissue sections, the prevalent expression patterns supported the contrasting metabolic behavior of cancer cells vs. tumor fibroblasts. The monocarboxylate/lactate transporter 1 (MCT1) was up-regulated in all the cell lines under hypoxic conditions, but it was suppressed under acidic conditions. The mitochondrial DNA (mtDNA) content per cell decreased significantly in the A549 cancer cell line under hypoxia, but it increased in the MRC5 fibroblasts. Taking into account these findings, we suggest that, under hypoxia, cancer cells intensify the anaerobic direction in glycolysis, while normal fibroblasts prefer to seek energy by intensifying the aerobic use of the available oxygen. [ABSTRACT FROM AUTHOR]

Low plasma 25-hydroxy-vitamin D (25OHD) and high levels of parathyroid hormone (PTH) are associated with obesity and could play a role in the occurrence of complications such as insulin resistance. The objective of the study was to evaluate whether the relationship between 25OHD status and phosphocalcic parameters differs between metabolically healthy obese (MHO) and insulin-resistant obese (IRO). This cross-sectional study included 158 consecutive adults (121 females) with obesity (body mass index (BMI) 35.15 ± 2.8 kg/m2), aged 43.21 ± 13.6 years. Serum 25OHD, calcemia, phosphatemia, PTH, plasma lipids, fasting plasma glucose, insulin levels, and body composition were measured. Participants were classified as MHO ( n = 65) or IRO ( n = 93) based on homeostatic model assessment insulin-resistance value. IRO patients had a higher BMI ( p = 0.001), waist circumference ( p = 0.03), and trunk fat mass ( p = 0.007) than MHO patients. Mean HbA1c ( p = 0.03), triglycerides ( p = 0.02), and hsCRP ( p = 0.04) plasmatic levels were increased in the IRO group. No between-group difference was found on 25OHD, PTH, calcium, or phosphorus plasmatic levels. Only age-predicted 25OHD levels were identified among IRO participants, whereas no factors were identified in MHO. No predictive factors of PTH plasmatic level were identified in the IRO and MHO groups. Although MHO and IRO patients have different metabolic profiles, we did not detect any difference regarding either 25OHD or PTH. Insulin resistance was not a predictive factor of vitamin D status. Our results confirm the absence of link between vitamin D status and insulin resistance in moderate obesity. [ABSTRACT FROM AUTHOR]

Over the last 50 years, Bengt Saltin's contributions to our understanding of physiology of the circulation, the matching of the circulation to muscle metabolism, and the underlying mechanisms that set the limits for exercise performance were enormous. His research addressed the key questions in the field using sophisticated experimental methods including field expeditions. From the Dallas Bedrest Study to the 1-leg knee model to the physiology of lifelong training, his prodigious body of work was foundational in the field of exercise physiology and his leadership propelled integrative human physiology into the mainstream of biological sciences. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Carbohydrate mouth rinsing can improve endurance exercise performance and is most ergogenic when exercise is completed in the fasted state. This strategy may also be beneficial to increase exercise capacity and the energy deficit achieved during moderate-intensity exercise relevant to weight control when performed after an overnight fast. Eighteen healthy men (mean (SD); age, 23 (4) years; body mass index, 23.1 (2.4) kg·m−2) completed a familiarisation trial and 3 experimental trials. After an overnight fast, participants performed 60 min of treadmill walking at a speed that equated to a rating of perceived exertion of 13 ('fairly hard'). Participants manually adjusted the treadmill speed to maintain this exertion. Mouth rinses for the experimental trials contained either a 6.4% maltodextrin solution with sweetener (CHO), a taste-matched placebo (PLA), or water (WAT). Appetite ratings were collected using visual analogue scales and exercise energy expenditure and substrate oxidation were calculated from online gas analysis. Increased walking distance during CHO and PLA induced greater energy expenditure compared with WAT (mean difference (90% confidence interval); 79 (60) kJ, P = 0.035, d = 0.24; and 90 (63) kJ, P = 0.024, d = 0.27, respectively). Appetite area under the curve was lower in CHO and PLA than WAT (8 (6) mm, P = 0.042, d = 0.43; and 6 (8) mm, P = 0.201, d = 0.32, respectively). Carbohydrate oxidation was higher in CHO than PLA and WAT (7.3 (6.7) g, P = 0.078, d = 0.47; and 10.1 (6.5) g, P = 0.015, d = 0.81, respectively). This study provides novel evidence that mouth rinsing with a sweetened solution may promote a greater energy deficit during moderate-exertion walking exercise by increasing energy expenditure and decreasing appetite. A placebo effect may have contributed to these benefits. [ABSTRACT FROM AUTHOR]

This study investigated substrate oxidation in concentric and eccentric cycling matched for aerobic power output in the postprandial state. Energy expenditure, respiratory exchange ratio, and fat and carbohydrate oxidation rates were measured at rest and after 15, 30, and 45 min of eccentric and concentric cycling in 12 men. Absolute and relative aerobic power output and energy expenditure were similar during concentric and eccentric exercise. No effect of exercise modality was observed for substrate metabolism. [ABSTRACT FROM AUTHOR]

It has been known for centuries that regularly performed exercise has beneficial effects on metabolic health. Owing to its central role in locomotion and the fact that it accounts for a large majority of whole-body glucose disposal and fatty acid oxidation, the effects of exercise on skeletal muscle has been a central focus in exercise physiology research. With this being said it is becoming increasingly well recognized that both adipose tissue and liver metabolism are robustly modified by exercise, especially in conditions of obesity and insulin resistance. One of the difficult questions to address is if the effects of exercise are direct or occur secondary to exercise-induced weight loss. The purpose of this review is to highlight recent work that has attempted to tease out the protective effects of exercise, or intrinsic aerobic capacity, against metabolic and inflammatory challenges as it relates to the treatment and prevention of obesity and insulin resistance. Recent studies reporting improvements in liver and adipose tissue insulin action following a single bout of exercise will also be discussed. The research highlighted in this review sheds new insight into protective, anti-inflammatory effects of exercise that occur largely independent of changes in adiposity and body weight. [ABSTRACT FROM AUTHOR]

Physical activity has the potential to reduce cardiometabolic risk factors but evaluation of different intensities of physical activity and the mechanisms behind their health effects still need to be fully established. This study examined the effects of sedentary behaviour, light-intensity training, and high-intensity interval training on biometric indices, glucose and lipid metabolism, inflammatory and oxidative stress markers, and vascular and cardiac function in adult rats. Rats (12 weeks old) were randomly assigned to 1 of 4 groups: control (CTL; no exercise), sedentary (SED; no exercise and housed in small cages to reduce activity), light-intensity trained (LIT; four 30-min exercise bouts/day at 8 m/min separated by 2-h rest period, 5 days/week), and high-intensity interval trained (HIIT, four 2.5-min work bouts/day at 50 m/min separated by 3-min rest periods, 5 days/week). After 12 weeks of intervention, SED had greater visceral fat accumulation ( p < 0.01) and slower cardiac conduction ( p = 0.04) compared with the CTL group. LIT and HIIT demonstrated beneficial changes in body weight, visceral and epididymal fat weight, glucose regulation, low-density lipoprotein cholesterol, total cholesterol, and mesenteric vessel contractile response compared with the CTL group ( p < 0.05). LIT had significant improvements in insulin sensitivity and cardiac conduction compared with the CTL and SED groups whilst HIIT had significant improvements in systolic blood pressure and endothelium-independent vasodilation to aorta and mesenteric artery compared with the CTL group ( p < 0.05). LIT and HIIT induce health benefits by improving traditional cardiometabolic risk factors. LIT improves cardiac health while HIIT promotes improvements in vascular health. [ABSTRACT FROM AUTHOR]

Cytochrome P450 enzyme 2D6 (CYP2D6) is an important member of the cytochrome P450 enzyme superfamily, with more than 100 CYP2D6 allelic variants being previously reported. The aim of this study was to assess the catalytic characteristics of 25 alleles ( CYP2D6.1 and 24 CYP2D6 variants) and their effects on the metabolism of propafenone in vitro. Twenty-five CYP2D6 alleles were expressing in 21 Spodoptera frugiperda ( Sf) insect cells, and each variant was evaluated using propafenone as the substrate. Reactions were performed at 37 °C with 1-100 μmol/L propafenone for 30 min. After termination, the product 5-OH-propafenone was extracted and used for signal collection by ultra-performance liquid chromatography (UPLC). Compared with wild type CYP2D6.1, the intrinsic clearance ( Vmax and Km) values of all variants were significantly altered. Three variants ( CYP2D6.87, CYP2D6.90, CYP2D6.F219S) exhibited markedly increased intrinsic clearance values (129% to 165%), whereas 21 variants exhibited significantly decreased values (16% to 85%) due to increased Km and (or) decreased Vmax values. These results indicated that the majority of tested alleles had significantly altered catalytic activity towards propafenone hydroxylation in this expression system. Attention should be paid to subjects carrying these rare alleles when treated with propafenone. [ABSTRACT FROM AUTHOR]

The aim of the present study was to assess if low and moderate doses of caffeine delivered in a carbohydrate-electrolyte solution (CES) late in exercise improved time-trial (TT) performance. Fifteen (11 male, 4 female) cyclists (age, 22.5 ± 0.9 years; body mass, 69.3 ± 2.6 kg; peak oxygen consumption, 64.6 ± 1.9 mL·min−1·kg−1) completed 4 double-blinded randomized trials. Subjects completed 120 min of cycling at ∼60% peak oxygen consumption with 5 interspersed 120-s intervals at ∼82% peak oxygen consumption, immediately followed by 40-s intervals at 50 W. Following 80 min of cycling, subjects either ingested a 6% CES (PL), a CES with 100 mg (low dose, 1.5 ± 0.1 mg·kg body mass−1) of caffeine (CAF1), or a CES with 200 mg (moderate dose, 2.9 ± 0.1 mg·kg body mass−1) of caffeine (CAF2). Following the 120-min cycling challenge, cyclists completed a 6-kJ·kg body mass−1 TT. There was no difference between respiratory, heart rate, glucose, free fatty acid, body mass, hematocrit, or urine specific gravity measurements between treatments. The CAF2 (26:36 ± 0:22 min:s) TT was completed faster than CAF1 (27:36 ± 0:32 min:s, p < 0.05) and both CAF1 and CAF2 TTs were completed faster than PL (28:41 ± 0:38 min:s, p < 0.05). Blood lactate was similar between trials and rose to a greater extent during the TT ( p < 0.05). In summary, both doses of caffeine delivered late in exercise improved TT performance over the PL trial and the moderate dose (CAF2) improved performance to a greater extent than the low dose (CAF1). [ABSTRACT FROM AUTHOR]

The timing of morning endurance competition may limit proper pre-race fueling and resulting performance. A nighttime, pre-sleep nutritional strategy could be an alternative method to target the metabolic and hydrating needs of the early morning athlete without compromising sleep or gastrointestinal comfort during exercise. Therefore, the purpose of this investigation was to examine the acute effects of pre-sleep chocolate milk (CM) ingestion on next-morning running performance, metabolism, and hydration status. Twelve competitive female runners and triathletes (age, 30 ± 7 years; peak oxygen consumption, 53 ± 4 mL·kg−1·min−1) randomly ingested either pre-sleep CM or non-nutritive placebo (PL) ∼30 min before sleep and 7-9 h before a morning exercise trial. Resting metabolic rate (RMR) was assessed prior to exercise. The exercise trial included a warm-up, three 5-min incremental workloads at 55%, 65%, and 75% peak oxygen consumption, and a 10-km treadmill time trial (TT). Physiological responses were assessed prior, during (incremental and TT), and postexercise. Paired t tests and magnitude-based inferences were used to determine treatment differences. TT performances were not different ('most likely trivial' improvement with CM) between conditions (PL: 52.8 ± 8.4 min vs CM: 52.8 ± 8.0 min). RMR was 'likely' increased (4.8%) and total carbohydrate oxidation (g·min−1) during exercise was 'possibly' or likely increased (18.8%, 10.1%, 9.1% for stage 1-3, respectively) with CM versus PL. There were no consistent changes to hydration indices. In conclusion, pre-sleep CM may alter next-morning resting and exercise metabolism to favor carbohydrate oxidation, but effects did not translate to 10-km running performance improvements. [ABSTRACT FROM AUTHOR]

The anabolic effects of nutrition on skeletal muscle may depend on adequate skeletal muscle perfusion, which is impaired in older people. Cocoa flavanols have been shown to improve flow-mediated dilation, an established measure of endothelial function. However, their effect on muscle microvascular blood flow is currently unknown. Therefore, the objective of this study was to explore links between the consumption of cocoa flavanols, muscle microvascular blood flow, and muscle protein synthesis (MPS) in response to nutrition in older men. To achieve this objective, leg blood flow (LBF), muscle microvascular blood volume (MBV), and MPS were measured under postabsorptive and postprandial (intravenous Glamin (Fresenius Kabi, Germany), dextrose to sustain glucose ~7.5 mmol·L-1) conditions in 20 older men. Ten of these men were studied with no cocoa flavanol intervention and a further 10 were studied with the addition of 350mgof cocoa flavanols at the same time that nutrition began. Leg (femoral artery) blood flow was measured by Doppler ultrasound, muscle MBV by contrast-enhanced ultrasound using Definity (Lantheus Medical Imaging, Mass., USA) perflutren contrast agent and MPS using [1, 2-13C2]leucine tracer techniques. Our results show that although older individuals do not show an increase in LBF or MBV in response to feeding, these absent responses are apparent when cocoa flavanols are given acutely with nutrition. However, this restoration in vascular responsiveness is not associated with improved MPS responses to nutrition. We conclude that acute cocoa flavanol supplementation improves muscle macro- and microvascular responses to nutrition, independently of modifying muscle protein anabolism. [ABSTRACT FROM AUTHOR]

Dexamethasone is an anti-inflammatory glucocorticoid that may alter glucose and lipid homeostasis when administered in high doses or for long periods of time. Omega-3 fatty acids, present in fish oil (FO), can be used as potential modulators of intermediary glucose and lipid metabolism. Herein, we evaluate the effects of FO supplementation (1 g·kg-1 body weight (BW)) on glucose and lipid metabolism in rats treated with dexamethasone (0.5 mg·kg-1 BW) for 15 days. Adult male Wistar rats were distributed among 4 groups: control (saline, 1 mL·kg-1 BW and mineral oil, 1 g·kg-1 BW), DEX (dexamethasone and mineral oil), FO (fish oil and saline), and DFO (fish oil and dexamethasone). Dexamethasone and saline were administered intraperitoneally, and fish oil and mineral oil were administered by gavage. We evaluated functional and molecular parameters of lipid and glycemic profiles at 8 days and at the end of treatment. FO supplementation increased hepatic docosahexaenoic acid (DEX: 5.6% ± 0.7%; DFO: 10.5% ± 0.8%) and eicosapentaenoic acid (DEX: 0.3% ± 0.0%; DFO: 1.3% ± 0.1%) contents and attenuated the increase of plasma triacylglycerol, total cholesterol, and non-high-density lipoprotein cholesterol concentrations in DFO rats compared with DEX rats. These effects seem not to depend on hepatic expression of insulin receptor substrate 1, protein kinase B, peroxisome proliferator-activated receptor γ coactivator 1-α, and peroxisome proliferator-activated receptor γ. There was no effect of supplementation on body weight loss, fasting glycemia, and glucose tolerance in rats treated with dexamethasone. In conclusion, we show that FO supplementation for 15 days attenuates the dyslipidemia induced by dexamethasone treatment. [ABSTRACT FROM AUTHOR]

This study analyzed the effect of 4 weeks of jumping interval training (JIT), included in endurance training, on neuromuscular and physiological parameters. Eighteen recreational runners, randomized in control and experimental groups, performed 40 min of running at 70% of velocity at peak oxygen uptake, for 3 times per week. Additionally, the experimental group performed the JIT twice per week, which consisted of 4 to 6 bouts of continuous vertical jumps (30 s) with 5-min intervals. Three days before and after the training period, the countermovement (CMJ) and continuous jump (CJ30), isokinetic and isometric evaluation of knee extensors/flexors, progressive maximal exercise, and submaximal constant-load exercise were performed. The JIT provoked improvement in neuromuscular performance, indicated by ( i) increased jump height (4.7%; effect size (ES) = 0.99) and power output (≈3.7%; ES ≈ 0.82) of CMJ and rate of torque development of knee extensors in isometric contraction (29.5%; ES = 1.02); ( ii) anaerobic power and capacity, represented by the mean of jump height (7.4%; ES = 0.8), and peak power output (PPO) (5.6%; ES = 0.73) of the first jumps of CJ30 and the mean of jump height (10.2%, ES = 1.04) and PPO (9.5%, ES = 1.1), considering all jumps of CJ30; and ( iii) aerobic power and capacity, represented by peak oxygen uptake (9.1%, ES = 1.28), velocity at peak oxygen uptake (2.7%, ES = 1.11), and velocity corresponding to the onset of blood lactate accumulation (9.7%, ES = 1.23). These results suggest that the JIT included in traditional endurance training induces moderate to large effects on neuromuscular and physiological parameters. [ABSTRACT FROM AUTHOR]

Diabetes is a chronic metabolic disease with a high prevalence worldwide. Diabetes and insulin resistance are associated with the development of cardiovascular and nervous diseases. The development of these disorders reflects complex pathological processes in which the oxidative stress caused by reactive oxygen species (ROS) and reactive nitrogen species (RNS) plays a pivotal role. It is widely accepted that diabetes impairs endothelial nitric oxide synthase (eNOS) activity and increases the production of ROS, thus resulting in diminished NO bioavailability and increased oxidative stress. Alpha-lipoic acid (LA) possesses beneficial effects both in the prevention and in the treatment of diabetes. LA is a potent antioxidant with insulin-mimetic and anti-inflammatory activity. LA in the diet is quickly absorbed, transported to the intracellular compartments, and reduced to dihydrolipoic acid (DHLA) under the action of enzymes. LA, which plays an essential role in mitochondrial bioenergetic reactions, has drawn considerable attention as an antioxidant for use in managing diabetic complications such as retinopathy, neuropathy and other vascular diseases. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Elevated levels of plasma free fatty acids (FFA), which are commonly found in obesity, induce insulin resistance. FFA activate protein kinases including the proinflammatory IκBα kinase β (IKKβ), leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and impaired insulin signaling. To test whether resveratrol, a polyphenol found in red wine, prevents FFA-induced insulin resistance, we used a hyperinsulinemic-euglycemic clamp with a tracer to assess hepatic and peripheral insulin sensitivity in overnight-fasted Wistar rats infused for 7 h with saline, Intralipid plus 20 U·mL−1 heparin (IH; triglyceride emulsion that elevates FFA levels in vivo; 5.5 μL·min−1) with or without resveratrol (3 mg·kg−1·h−1), or resveratrol alone. Infusion of IH significantly decreased glucose infusion rate (GIR; P < 0.05) and peripheral glucose utilization ( P < 0.05) and increased endogenous glucose production (EGP; P < 0.05) during the clamp compared with saline infusion. Resveratrol co-infusion, however, completely prevented the effects induced by IH infusion: it prevented the decreases in GIR ( P < 0.05 vs. IH), peripheral glucose utilization ( P < 0.05 vs. IH), and insulin-induced suppression of EGP ( P < 0.05 vs. IH). Resveratrol alone had no effect. Furthermore, IH infusion increased serine (307) phosphorylation of IRS-1 in soleus muscle (∼30-fold, P < 0.001), decreased total IRS-1 levels, and decreased IκBα content, consistent with activation of IKKβ. Importantly, all of these effects were abolished by resveratrol ( P < 0.05 vs. IH). These results suggest that resveratrol prevents FFA-induced hepatic and peripheral insulin resistance and, therefore, may help mitigate the health consequences of obesity. [ABSTRACT FROM AUTHOR]

The incidence of type 2 diabetes is increasing rapidly worldwide, and the development of novel anti-diabetic drugs is emerging. However, most anti-diabetic drugs cannot be used in patients with hepatic dysfunction, renal disease, and heart disease, which makes pharmacological therapy of type 2 diabetes complicated. Despite continued introduction of novel agents, the search for an ideal drug that is useful as both a hypoglycemic agent and to reduce diabetes-related complications remains elusive. Berberine is an isoquinoline alkaloid extract that has shown promise as a hypoglycemic agent in the management of diabetes in animal and human studies. Mechanistic studies have revealed beneficial effects of berberine on diabetes-related complications. Although there have been few clinical reports of the anti-diabetic effects of berberine, little documentation of adverse effects in humans positions it as a potential candidate drug to treat type 2 diabetes. In the present review, the anti-diabetic mechanism of berberine, its effect on diabetes-related complications, and its recent use in human clinical studies is highlighted. In addition, we summarize the different treatments for type 2 diabetes in adults and children. [ABSTRACT FROM AUTHOR]

The metabolic interplay between hosts and viruses plays a crucial role in determining the outcome of viral infection. Viruses reorchestrate the host's primary metabolic gene networks, including genes associated with mevalonate and isoprenoid synthesis, to acquire the necessary energy and structural components for their viral life cycles. Recent work has demonstrated that the interferon-mediated antiviral response suppresses the sterol pathway through production of a signalling molecule, 25-hydroxycholesterol (25HC). This oxysterol has been shown to exert multiple effects, both through incorporation into host cellular membranes as well as through transcriptional control. Herein, we summarize our current understanding of the multifunctional roles of 25HC in the mammalian innate antiviral response. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Microbiology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Stimulation of the energy sensor AMP-activated kinase (AMPK) has been viewed as a targeted approach to increase glucose uptake by skeletal muscle and control blood glucose homeostasis. Rosemary extract (RE) has been reported to activate AMPK in hepatocytes and reduce blood glucose levels in vivo but its effects on skeletal muscle are not known. In the present study, we examined the effects of RE and the mechanism of regulation of glucose uptake in muscle cells. RE stimulated glucose uptake in L6 myotubes in a dose- and time-dependent manner. Maximum stimulation was seen with 5 μg/mL of RE for 4 h (184% ± 5.07% of control, p < 0.001), a response comparable to maximum insulin (207% ± 5.26%, p < 0.001) and metformin (216% ± 8.77%, p < 0.001) stimulation. RE did not affect insulin receptor substrate 1 and Akt phosphorylation but significantly increased AMPK and acetyl-CoA carboxylase phosphorylation. Furthermore, the RE-stimulated glucose uptake was significantly reduced by the AMPK inhibitor compound C, but remained unchanged by the PI3K inhibitor, wortmannin. RE did not affect GLUT4 or GLUT1 glucose transporter translocation in contrast with a significant translocation of both transporters seen with insulin or metformin treatment. Our study is the first to show a direct effect of RE on muscle cell glucose uptake by a mechanism that involves AMPK activation. [ABSTRACT FROM AUTHOR]

The acute relationship between substrate oxidation as measured by respiratory exchange ratio (RER) and food intake (FI) has not been defined. The purpose of the study was to determine acute relationships between RER, modified by exercise and a glucose load, and FI and net energy balance (NEB) in physically active normal-weight boys and men. In a crossover design, 15 boys (aged 9-12 years) and 15 men (aged 20-30 years) were randomly assigned to 4 conditions: ( i) water and rest, ( ii) glucose-drink and rest, ( iii) water and exercise, and ( iv) glucose-drink and exercise. Indirect calorimetry was used to determine RER, energy expenditure, and carbohydrate and fat oxidation. Subjective appetite and blood glucose were also measured. RER was higher after glucose (0.91 ± 0.01) compared with water (0.87 ± 0.01) ( p < 0.0001), and after exercise (0.91 ± 0.01) compared with rest (0.88 ± 0.01) ( p = 0.0043) in men (0.91 ± 0.01) compared with boys (0.88 ± 0.01) ( p = 0.0002). FI (kcal·m−2) did not differ between boys and men. Glucose (582 ± 24 kcal·m−2) reduced FI compared with water (689 ± 25 kcal·m−2) ( p < 0.0001), and further decreased FI when combined with exercise (554 ± 34 kcal·m−2) ( p = 0.0303). NEB was reduced with exercise (573 ± 25 kcal·m−2) compared with the sedentary condition (686 ± 24 kcal·m−2) ( p < 0.0001), but was higher after the glucose drink (654 ± 27 kcal·m−2) compared with water (605 ± 25 kcal·m−2) ( p = 0.0267). No correlations were found between RER and FI or NEB in boys and men, except in the control condition of resting with water. In conclusion, the short-term modification of substrate oxidation by glucose and/or exercise in normal weight and active boys and men did not affect FI and NEB. [ABSTRACT FROM AUTHOR]

Most sprint interval training (SIT) research involves cycling as the mode of exercise and whether running SIT elicits a similar excess postexercise oxygen consumption (EPOC) response to cycling SIT is unknown. As running is a more whole-body-natured exercise, the potential EPOC response could be greater when using a running session compared with a cycling session. The purpose of the current study was to determine the acute effects of a running versus cycling SIT session on EPOC and whether potential sex differences exist. Sixteen healthy recreationally active individuals (8 males and 8 females) had their gas exchange measured over ∼2.5 h under 3 experimental sessions: ( i) a cycle SIT session, ( ii) a run SIT session, and ( iii) a control (CTRL; no exercise) session. Diet was controlled. During exercise, both SIT modes increased oxygen consumption (cycle: male, 1.967 ± 0.343; female, 1.739 ± 0.296 L·min−1; run: male, 2.169 ± 0.369; female, 1.791 ± 0.481 L·min−1) versus CTRL (male, 0.425 ± 0.065 L·min−1; female, 0.357 ± 0.067; P < 0.001), but not compared with each other ( P = 0.234). In the first hour postexercise, oxygen consumption was still increased following both run (male, 0.590 ± 0.065; female, 0.449 ± 0.084) and cycle SIT (male, 0.556 ± 0.069; female, 0.481 ± 0.110 L·min−1) versus CTRL and oxygen consumption was maintained through the second hour postexercise (CTRL: male, 0.410 ± 0.048; female, 0.332 ± 0.062; cycle: male, 0.430 ± 0.047; female, 0.395 ± 0.087; run: male, 0.463 ± 0.051; female, 0.374 ± 0.087 L·min−1). The total EPOC was not significantly different between modes of exercise or males and females ( P > 0.05). Our data demonstrate that the mode of exercise during SIT (cycling or running) is not important to O2 consumption and that males and females respond similarly. [ABSTRACT FROM AUTHOR]

Solid tumors are characterized by a microenvironment that is highly acidic, while intracellular pH (pHi) is normal or even elevated. This is the result of elevated metabolic rates in the highly proliferative cancer cells, in conjunction with often greatly increased rates of net cellular acid extrusion. Studies in various cancers have suggested that while the acid extrusion mechanisms employed are generally the same as those in healthy cells, the specific transporters upregulated vary with the cancer type. The main such transporters include Na+/H+ exchangers, various HCO3− transporters, H+ pumps, and lactate-H+ cotransporters. The mechanisms leading to their dysregulation in cancer are incompletely understood but include changes in transporter expression levels, trafficking and membrane localization, and posttranslational modifications. In turn, accumulating evidence has revealed that in addition to supporting their elevated metabolic rate, their increased acid efflux capacity endows the cancer cells with increased capacity for invasiveness, proliferation, and chemotherapy resistance. The pancreatic duct exhibits an enormous capacity for acid-base transport, rendering pHi dysregulation a potentially very important topic in pancreatic ductal adenocarcinoma (PDAC). PDAC - accounting for about 90% of all pancreatic cancers - has one of the highest cancer mortality rates known, and new diagnostic and treatment options are highly needed. However, very little is known about whether pH regulation is altered in PDAC and, if so, the possible role of this in cancer development. Here, we review current models for pancreatic acid-base transport and pH homeostasis and summarize current views on acid-base dysregulation in cancer, focusing where possible on the few studies to date in PDAC. Finally, we present new data-mining analyses of acid-base transporter expression changes in PDAC and discuss essential directions for future work. [ABSTRACT FROM AUTHOR]

Copyright of Biochemistry & Cell Biology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Metabolic disturbances and oxidative stress have been highlighted as potential causative factors for the development of diabetic cardiomyopathy. The β-blocker metoprolol is known to improve function in the diabetic rat heart and ameliorates the sequelae associated with oxidative stress, without lowering oxidative stress. The antioxidant ascorbic acid is known to improve function in the diabetic rat heart. We tested whether a combination of ascorbic acid and metoprolol treatment would improve function further than each drug individually. Control and streptozotocin-induced diabetic Wistar rats were treated with metoprolol (15 mg·(kg body mass)−1·day−1, via an osmotic pump) and (or) ascorbic acid (1000 mg·(kg body mass)−1·day−1, via their drinking water). To study the effect of treatment on the development of dysfunction, we examined time points before (5 weeks diabetic) and after (7 weeks diabetic) development of overt systolic dysfunction. Echocardiography and working-heart-perfusion were used to assess cardiac function. Blood and tissue samples were collected to assess the severity of disease and oxidative stress. While both drugs improved function, only ascorbic acid had effects on oxidative damage. Combination treatment had a more pronounced improvement in function. Our β-blocker + antioxidant treatment strategy focused on oxidative stress, not diabetes specifically; therefore, it may prove useful in other diseases where oxidative stress contributes to the pathology. [ABSTRACT FROM AUTHOR]

We evaluated the effects of oral glycerol supplementation on trained rats fed a normal diet. Wistar rats were distributed among 6 groups in a completely randomized 2 × 3 factorial design. The animals were subjected to 6 weeks of aerobic training. In the last 4 weeks, the animals' diet was supplemented with saline, glucose, or glycerol. Data were subjected to one-way analysis of variance (ANOVA) followed by a Student-Newmann-Keuls test, with values for P < 0.05 considered statistically significant. The change in body mass was lower in the trained groups, and their food and water consumption were higher. Glycerol supplementation resulted in an increase in the levels of triacylglycerol (TAG) and total cholesterol, as well as in the area and diameter of adipocytes. When associated with training, these parameters were similar to those of other trained groups. Levels of low-density lipoprotein + very-low-density lipoprotein cholesterol decreased in the trained animals that received glycerol compared with the non-trained ones. Glycerol consumption caused a reduction in food intake and increased the villous:crypt (V:C) ratio. No changes in glycemia, high density lipoproteins, or density of adipocytes were observed. Supplementation with glycerol together with aerobic physical training promoted beneficial metabolic effects. However, in non-trained rats glycerol increased the diameter and area of adipocytes, as well as the levels of TAG and total cholesterol. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Animal Science is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Modification of mitochondrial content demands the synthesis of hundreds of proteins encoded by nuclear and mitochondrial genomes. The responsibility for coordination of this process falls to nuclear-encoded master regulators of transcription. DNA-binding proteins and coactivators integrate information from energy-sensing pathways and hormones to alter mitochondrial gene expression. In mammals, the signaling cascade for mitochondrial biogenesis can be described as follows: hormonal signals and energetic information are sensed by protein-modifying enzymes that in turn regulate the post-translational modification of transcription factors. Once activated, transcription-factor complexes form on promoter elements of many of the nuclear-encoded mitochondrial genes, recruiting proteins that remodel chromatin and initiate transcription. One master regulator in mammals, PGC-1α, is well studied because of its role in determining the metabolic phenotype of muscles, but also due to its importance in mitochondria-related metabolic diseases. However, relatively little is known about the role of this pathway in other vertebrates. These uncertainties raise broader questions about the evolutionary origins of the pathway and its role in generating the diversity in muscle metabolic phenotypes seen in nature. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Zoology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cachexia is a wasting syndrome that may accompany a plethora of diseases, including cancer, chronic obstructive pulmonary disease, aids, and rheumatoid arthritis. It is associated with central and systemic increases of pro-inflammatory factors, and with decreased quality of life, response to pharmacological treatment, and survival. At the moment, there is no single therapy able to reverse cachexia many symptoms, which include disruption of intermediary metabolism, endocrine dysfunction, compromised hypothalamic appetite control, and impaired immune function, among other. Growing evidence, nevertheless, shows that chronic exercise, employed as a tool to counteract systemic inflammation, may represent a low-cost, safe alternative for the prevention/attenuation of cancer cachexia. Despite the well-documented capacity of chronic exercise to counteract sustained disease-related inflammation, few studies address the effect of exercise training in cancer cachexia. The aim of the present review was hence to discuss the results of cachexia treatment with endurance training. As opposed to resistance exercise, endurance exercise may be performed devoid of equipment, is well tolerated by patients, and an anti-inflammatory effect may be observed even at low-intensity. The decrease in inflammatory status induced by endurance protocols is paralleled by recovery of various metabolic pathways. The mechanisms underlying the response to the treatment are considered. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Obesity and high-fructose corn syrup (HFCS)-sweetened beverages are associated with an increased risk of chronic disease, but it is not clear whether obese (Ob) individuals are more susceptible to the detrimental effects of HFCS-sweetened beverages. The purpose of this study was to examine the endocrine and metabolic effects of consuming HFCS-sweetened beverages, and whether weight classification (normal weight (NW) vs. Ob) influences these effects. Ten NW and 10 Ob men and women who habitually consumed ≤355 mL per day of sugar-sweetened beverages were included in this study. Initially, the participants underwent a 4-h mixed-meal test after a 12-h overnight fast to assess insulin sensitivity, pancreatic and gut endocrine responses, insulin secretion and clearance, and glucose, triacylglycerol, and cholesterol responses. Next, the participants consumed their normal diet ad libitum, with 1065 mL per day (117 g·day-1) of HFCS-sweetened beverages added for 2 weeks. After the intervention, the participants repeated the mixed-meal test. HFCS-sweetened beverages did not significantly alter body weight, insulin sensitivity, insulin secretion or clearance, or endocrine, glucose, lipid, or cholesterol responses in either NW or Ob individuals. Regardless of previous diet, Ob individuals, compared with NW individuals, had ∼28% lower physical activity levels, 6%-9% lower insulin sensitivity, 12%-16% lower fasting high-density-lipoprotein cholesterol concentrations, 84%-144% greater postprandial triacylglycerol concentrations, and 46%-79% greater postprandial insulin concentrations. Greater insulin responses were associated with reduced insulin clearance, and there were no differences in insulin secretion. These findings suggest that weight classification does not influence the short-term endocrine and metabolic effects of HFCS-sweetened beverages. [ABSTRACT FROM AUTHOR]

We investigated the effects of consuming a high-carbohydrate meal (HC), high-fat meal (HF), or no meal (CON) following exercise on fat and carbohydrate oxidation (FAT-OX, CHO-OX) in women with differing levels of body fat. Healthy, physically active females were divided into a Lower Fat (<25% fat, n = 10) or Higher Fat (>25% fat, n = 9) group and tested on 4 occasions. During session 1, body composition and maximal oxygen consumption were determined. During 3 treatment sessions, subjects preformed treadmill exercise at 55% of maximal oxygen consumption until 350 kcal were expended. At 10 min postexercise subjects consumed a liquid meal standardized to provide energy equal to 20% of 24-h energy expenditure plus the 350 kcal of exercise. The HC meal comprised 64% carbohydrate, 21.6% fat, and 14.4% protein. The HF meal comprised 24% carbohydrate, 62% fat, and 14% protein. CON consisted of water equal to the meal volume. During exercise and 2 h postexercise, expired gases were collected to determine FAT-OX and CHO-OX. During exercise CHO-OX was a significantly higher for the Lower Fat group and FAT-OX was significantly higher for the Lower Fat group for each of the meal conditions. A significant difference was observed across meal s ( p < 0.05) for CHO-OX (first hour) and for CHO-OX and FAT-OX (second hour) postexercise. There were no significant differences ( p > 0.05) between the Lower Fat and Higher Fat groups for either recovery period. In physically active females, the macronutrient composition of the postexercise meal affects substrate oxidation, but the level of body fat does not. [ABSTRACT FROM AUTHOR]

Glucose uptake and glycolysis are increased in the heart during ischemia, and this metabolic alteration constitutes an important contributing factor towards ischemic injury. Therefore, it is important to understand glucose uptake regulation in the ischemic heart. There are primarily 2 glucose transporters controlling glucose uptake into cardiac myocytes: GLUT1 and GLUT4. In the non-ischemic heart, insulin stimulates GLUT4 translocation to the sarcolemmal membrane, while both GLUT1 and GLUT4 translocation can occur following AMPK stimulation. Using a newly developed technique involving [3H]2-deoxyglucose, we measured glucose uptake in H9c2 ventricular myoblasts, and demonstrated that while insulin has no detectable effect on glucose uptake, phenformin-induced AMPK activation increases glucose uptake 2.5-fold. Furthermore, insulin treatment produced no discernible effect on either Akt serine 473 phosphorylation or AMPKα threonine 172 phosphorylation, while treatment with phenformin results in an increase in AMPKα threonine 172 phosphorylation, and a decrease in Akt serine 473 phosphorylation. Visualization of a dsRed-GLUT4 fusion construct in H9c2 cells by laser confocal microscopy showed that unlike insulin, AMPK activation did not redistribute GLUT4 to the sarcolemmal membrane, suggesting that AMPK may regulate glucose uptake via another glucose transporter. These studies suggest that AMPK is a major regulator of glucose uptake in cardiac myocytes. [ABSTRACT FROM AUTHOR]

This study compared accelerometer-measured physical activity by body placement to daily total energy expenditure (TEE) and activity energy expenditure (AEE) measured using doubly labeled water (DLW). Forty-nine adult participants wore accelerometers placed on the nondominant wrist, dominant wrist, and chest while also undergoing DLW assessments. In adjusted models, wrist-measured physical activity ( p  < 0.05), but not chest-measured physical activity ( p  > 0.05), was associated with TEE and AEE and explained a significant amount of variance that was not explained by age, sex, height, or body composition ( R 2 change = 0.04-0.08; all p  < 0.05). Accelerometer placement location is an important consideration when using accelerometry to provide information about energy expenditure.

Glucocorticoid (GC) excess alters glucose homeostasis and promotes modifications in murinometric and anthropometric parameters in rodents and humans, respectively. β-hydroxy-β-methylbutyrate (HMB), a leucine metabolite, has been proposed as a nutritional strategy for preventing muscle wasting, but few data regarding its effects on glucose homeostasis are available. Here, we analyzed whether the effects of GC excess on glucose homeostasis may be attenuated or exacerbated by the concomitant ingestion of HMB. Adult Wistar rats (90-days-old) were assigned to four groups: (1) vehicle treated (Ctl), (2) dexamethasone (DEX) treated (Dex), (3) HMB treated (Hmb), and (4) DEX plus HMB treated (DexHmb). Dex groups received DEX (1 mg·kg body weight (BW)−1, intraperitoneal) for 5 consecutive days. HMB groups ingested HMB (320 mg·kg BW−1, oral gavage) for the same 5 days. HMB ingestion did not attenuate the effects of DEX on food intake and body weight loss, changes in masses of several organs, insulin resistance, and glucose intolerance ( p > 0.05). In fact, in DexHmb rats, there was increased fasting glycemia and exacerbated glucose intolerance with the main effect attributed to DEX treatment ( p < 0.05). HMB exerted no attenuating effect on plasma triacylglycerol levels from DexHmb rats, but it seems to attenuate the lipolysis induced by β-adrenergic stimulation (20 μmol·L−1 isoproterenol) in fragments of retroperitoneal adipose tissue from DexHmb rats. Therefore, HMB does not attenuate the diabetogenic characteristics of GC excess. In fact, the data suggest that HMB may exacerbate GC-induced glucose intolerance. [ABSTRACT FROM AUTHOR]

Despite being a group of particular interest in considering relationships between genome size and metabolic parameters, bats have not been well studied from this perspective. This study presents new estimates for 121 'microbat' species from 12 families and complements a previous study on members of the family Pteropodidae ('megabats'). The results confirm that diversity in genome size in bats is very limited even compared with other mammals, varying approximately 2-fold from 1.63 pg in Lophostoma carrikeri to 3.17 pg in Rhinopoma hardwickii and averaging only 2.35 pg ± 0.02 SE (versus 3.5 pg overall for mammals). However, contrary to some other vertebrate groups, and perhaps owing to the narrow range observed, genome size correlations were not apparent with any chromosomal, physiological, flight-related, developmental, or ecological characteristics within the order Chiroptera. Genome size is positively correlated with measures of body size in bats, though the strength of the relationships differs between pteropodids ('megabats') and nonpteropodids ('microbats'). [ABSTRACT FROM AUTHOR]

Copyright of Genome is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study examined acute physiologic responses to a thermogenic nutritional supplement at rest, during exercise, and during recovery from exercise in women. Twelve women (mean ± SD age, 22.9 ± 3.1 years) were recruited for this randomized, double-blinded, placebo-controlled, crossover study. Each testing session consisted of 4 phases: 30 min of presupplementation resting, followed by the ingestion of the placebo or thermogenic nutritional supplement; 50 min of postsupplementation resting; 60 min of walking (at 3.2-4.8 km·h−1); and 50 min of postexercise resting. Energy expenditure (EE), oxygen consumption, respiratory exchange ratio (RER), oxygen (O2) pulse, and heart rate (HR) values were recorded during all 4 phases. Systolic (SBP) and diastolic (DBP) blood pressure were recorded during the rest, postsupplementation, and postexercise recovery phases; ratings of perceived exertion (RPE) were recorded only during exercise. There were no significant differences for EE, oxygen consumption, O2 pulse, HR, SBP, or DBP between the supplement and placebo during the presupplementation resting or postsupplementation phases. The RER, however, was higher with the supplement at 30 min postsupplementation. During exercise, EE and O2 pulse were 3%-6% greater with the supplement than placebo; there were no significant differences in RPE. Postexercise, EE, oxygen consumption, and DBP were 3%-7% greater with the supplement than placebo. These findings suggest that a thermogenic nutritional supplement, when combined with exercise, increases metabolic rate but has no effect on the perception of effort and results in only minimal changes in cardiovascular function. [ABSTRACT FROM AUTHOR]

The purpose of the present study was to examine the effects of a high- or low-carbohydrate (CHO) diet on performance, aerobic and anaerobic contribution, and metabolic responses during supramaximal exercise. Six physically-active men first performed a cycling exercise bout at 115% maximal oxygen uptake to exhaustion after following their normal diet for 48 h (∼50% of CHO, control test). Seventy-two hours after, participants performed a muscle glycogen depletion exercise protocol, followed by either a high- or low-CHO diet (∼70 and 25% of CHO, respectively) for 48 h, in a random, counterbalanced order. After the assigned diet period (48 h), the supramaximal cycling exercise bout (115% maximal oxygen consumption) to exhaustion was repeated. The low-CHO diet reduced time to exhaustion when compared with both the control and the high-CHO diet (−19 and −32%, respectively, p < 0.05). The reduced time to exhaustion following the low-CHO diet was accompanied by a lower total aerobic energy contribution (−39%) compared with the high-CHO diet ( p < 0.05). However, the aerobic and anaerobic energy contribution at the shortest time to exhaustion (isotime) was similar among conditions ( p > 0.05). The low-CHO diet was associated with a lower blood lactate concentration ( p < 0.05), with no effect on the plasma concentration of insulin, glucose and K+ ( p > 0.05). In conclusion, a low-CHO diet reduces both performance and total aerobic energy provision during supramaximal exercise. As peak K+ concentration was similar, but time to exhaustion shorter, the low-CHO diet was associated with an earlier attainment of peak plasma K+ concentration. [ABSTRACT FROM AUTHOR]