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Iwayama, K, Tanabe, Y, Yajima, K, Tanji, F, Onishi, T, and Takahashi, H. Preexercise high-fat meal following carbohydrate loading attenuates glycogen utilization during endurance exercise in male recreational runners. J Strength Cond Res XX(X): 000-000, 2022-This study aimed to investigate whether one preexercise high-fat meal can increase glycogen conservation during endurance exercise, as compared with one preexercise high-carbohydrate meal. Ten young male recreational runners (22.0 ± 0.6 years; 171.3 ± 0.9 cm; 58.3 ± 1.9 kg; maximal oxygen uptake [V̇o2max], 62.0 ± 1.6 ml·kg-1·min-1) completed 2 exercise trials after high-carbohydrate loading: eating a high-carbohydrate (CHO; 7% protein, 13% fat, 80% carbohydrate) meal or eating a high-fat (FAT; 7% protein, 42% fat, 52% carbohydrate) meal 3.5 hours before exercise. The order of the 2 trials was randomized, and the interval between trials was at least 1 week. The experimental exercise consisted of running on a treadmill for 60 minutes at 95% of each subject's lactate threshold. Muscle and liver glycogen content were assessed using noninvasive carbon magnetic resonance spectroscopy before the experimental meal as well as before and after exercise; respiratory gases were measured continuously during exercise. The respiratory exchange ratio during exercise was statistically lower in the FAT trial than in the CHO trial (p0.01). In addition, muscle (p0.05) and liver (p0.05) glycogen utilization during exercise was less in the FAT trial than in the CHO trial. Therefore, one high-fat meal following carbohydrate loading reduced muscle and liver glycogen use during the 60-minute exercise. These results suggest that this dietary approach may be applied as a strategy to optimize energy utilization during endurance exercise.

Exercise can improve sleep by reducing sleep latency and increasing slow-wave sleep (SWS). Some studies, however, report adverse effects of exercise on sleep architecture, possibly due to a wide variety of experimental conditions used. We examined the effect of exercise on quality of sleep using standardized exercise parameters and novel analytical methods. In a cross-over intervention study we examined the effect of 60 min of vigorous exercise at 60% $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 max on the metabolic state, assessed by core body temperature and indirect calorimetry, and on sleep quality during subsequent sleep, assessed by self-reported quality of sleep and polysomnography. In a novel approach, envelope analysis was performed to assess SWS stability. Exercise increased energy expenditure throughout the following sleep phase. The subjective assessment of sleep quality was not improved by exercise. Polysomnography revealed a shorter rapid eye movement latency and reduced time spent in SWS. Detailed analysis of the sleep electro-encephalogram showed significantly increased delta power in SWS (N3) together with increased SWS stability in early sleep phases, based on delta wave envelope analysis. Although vigorous exercise does not lead to a subjective improvement in sleep quality, sleep function is improved on the basis of its effect on objective EEG parameters.

It has been suggested that glycogen functions not only in carbohydrate energy storage, but also as molecular sensors capable of activating lipolysis. This study aimed to compare the variation in liver and muscle glycogen during the day due to different timing of exercise. Nine healthy young men participated in two trials in which they performed a single bout of exercise at 70% of their individual maximal oxygen uptake for 60 min in the post-absorptive (morning) or post-prandial (afternoon) state. Liver and muscles glycogen levels were measured using carbon magnetic resonance spectroscopy (13C MRS). Diurnal variations in liver and muscle glycogen compared to baseline levels were significantly different depending on the timing of exercise. The effect of the timing of exercise on glycogen fluctuation is known to be related to a variety of metabolic signals, and the results of this study will be useful for future research on energy metabolism.

Background Skipping breakfast has become a common trend that may lead to obesity and type 2 diabetes. Previous studies, which imposed a single incidence of breakfast skipping, did not observe any decrease in 24-h energy expenditure. Furthermore, the effects of breakfast skipping on diurnal blood glucose profiles over 24 h are contradictory. Objective The aim of this study was to clarify the influence of 6 consecutive days of breakfast skipping and sedentary behavior on energy metabolism and glycemic control. Methods Ten young men participated in 2 trials (with or without breakfast) that lasted for 6 consecutive days, and the 2 trials were conducted 1 wk apart with a repeated-measures design. During the meal intervention, each subject's blood glucose was measured using the continuous glucose monitoring system. If breakfast was skipped, subjects ate large meals at lunch and dinner such that the 24-h energy intake was identical to that of the 3-meal condition. At 2200 on the fifth day, the subjects entered a room-sized respiratory chamber, where they remained for 33 h, and were instructed to carry out sedentary behavior. Results The glucose levels were similar between the 2 meal conditions during the first 5 d of meal intervention, but the blood glucose at 2300 was higher in the breakfast-skipping condition than in the 3-meal condition. Breakfast skipping elevated postprandial glycemic response after lunch on the first day of meal intervention. On the sixth day, there were no significant differences in 24-h energy expenditure and substrate oxidation. When subjects remained in a metabolic chamber, the level of physical activity significantly decreased, glycemic stability slightly deteriorated, and mean blood glucose over 24 h was higher in the breakfast-skipping trial than in the 3-meal trial. Conclusions Sedentary lifestyle and repeated breakfast skipping caused abnormal glucose fluctuations, whereas 24-h energy metabolism remained unaffected. Clinical Trial Registry: This trial was registered at http://www.umin.ac.jp/english/ as UMIN000032346.

Known as metabolic flexibility, oxidized substrate is selected in response to changes in the nutritional state. Sleep imposes an extended duration of fasting, and oxidized substrates during sleep were assumed to progressively shift from carbohydrate to fat, thereby gradually decreasing the respiratory quotient (RQ). Contrary to this assumption, whole-room indirect calorimetry with improved time resolution revealed that RQ re-ascended prior to awakening, and nadir of RQ in non-obese young adults occurred earlier in women than men after bedtime. The transient decrease in RQ during sleep was blunted in metabolically inflexible men with smaller amplitude of diurnal rhythm in RQ. Similarly, the effect of 10 years difference in age on RQ became significant during sleep; the decrease in RQ during sleep was blunted in older subjects. Inter-individual difference in RQ become apparent during sleep, and it might serve as a window to gain insight into the early-stage pathogenesis of metabolic inflexibility.

Glycogen in tissues functions not only as carbohydrate reserves, but also as molecular sensors capable of activating signaling pathways in response to physical activity. While glycogen in the skeletal muscles is mainly a local energy substrate, glycogen in the liver serves as a glucose reserve to maintain normal blood glucose levels in the body, even during the sleep state. The aim of this study is to compare the diurnal variation of glycogen in the muscle and liver of human subjects under normal conditions. The glycogen content was measured in the muscle and liver of 10 young, healthy, male volunteers using 13 C MRS, a non-invasive technique. The subjects remained sedentary, and glycogen concentration was measured six times daily. Experimental meals were provided to achieve individual energy balance, estimated according to the energy requirement guideline for patients from Japan. The largest variation in muscle glycogen compared with 1 h after supper (20:00 on Day 1) was 3.1 ± 8.2 mmol/L (16:00 on Day 2). In the liver, however, the glycogen content decreased by 80.6 ± 40.4 mmol/L through the overnight fasting period (07:00 on Day 2). This study demonstrated that the glycogen content in the liver was significantly lower in the morning, while the glycogen content in the calf muscles underwent minimal diurnal variation. The overnight fast is a characteristic daily condition, in which liver glycogen content is low, whereas muscle glycogen content is relatively unaffected.

Glycogen in tissues functions not only as carbohydrate reserves, but also as molecular sensors capable of activating signaling pathways in response to physical activity. While glycogen in the skeletal muscles is mainly a local energy substrate, glycogen in the liver serves as a glucose reserve to maintain normal blood glucose levels in the body, even during the sleep state. The aim of this study is to compare the diurnal variation of glycogen in the muscle and liver of human subjects under normal conditions. The glycogen content was measured in the muscle and liver of 10 young, healthy, male volunteers using

Dynamic metabolic changes occur in the liver during the transition between fasting and feeding. Here we show that transient ER stress responses in the liver following feeding terminated by Sdf2l1 are essential for normal glucose and lipid homeostasis. Sdf2l1 regulates ERAD through interaction with a trafficking protein, TMED10. Suppression of Sdf2l1 expression in the liver results in insulin resistance and increases triglyceride content with sustained ER stress. In obese and diabetic mice, Sdf2l1 is downregulated due to decreased levels of nuclear XBP-1s, whereas restoration of Sdf2l1 expression ameliorates glucose intolerance and fatty liver with decreased ER stress. In diabetic patients, insufficient induction of Sdf2l1 correlates with progression of insulin resistance and steatohepatitis. Therefore, failure to build an ER stress response in the liver may be a causal factor in obesity-related diabetes and nonalcoholic steatohepatitis, for which Sdf2l1 could serve as a therapeutic target and sensitive biomarker., Endoplasmic reticulum (ER) stress has been proposed to play a role in metabolic diseases. Here, Sasako and colleagues identify stromal cell-derived factor 2 like 1 (Sdf2l1) as a regulator of the ER stress response to feeding in the liver, and suggest that its downregulation may promote diabetes and hepatic steatosis in humans.

M2a-subtype macrophage activation is known to be impaired in obesity, although the underlying mechanisms remain poorly understood. Herein, we demonstrate that, the IL-4/Irs2/Akt pathway is selectively impaired, along with decreased macrophage Irs2 expression, although IL-4/STAT6 pathway is maintained. Indeed, myeloid cell-specific Irs2-deficient mice show impairment of IL-4-induced M2a-subtype macrophage activation, as a result of stabilization of the FoxO1/HDAC3/NCoR1 corepressor complex, resulting in insulin resistance under the HF diet condition. Moreover, the reduction of macrophage Irs2 expression is mediated by hyperinsulinemia via the insulin receptor (IR). In myeloid cell-specific IR-deficient mice, the IL-4/Irs2 pathway is preserved in the macrophages, which results in a reduced degree of insulin resistance, because of the lack of IR-mediated downregulation of Irs2. We conclude that downregulation of Irs2 in macrophages caused by hyperinsulinemia is responsible for systemic insulin resistance via impairment of M2a-subtype macrophage activation in obesity., Obesity is associated with low-grade chronic inflammation. Here the authors show that the activation of anti-inflammatory M2a-subtype macrophages requires the IL4/Irs2/Akt pathway. Due to decreased Irs2 expression this pathway is impaired in obese mice thus leading to a defect in M2a activation.

Recently, incretin-related agents have been reported to attenuate insulin resistance in animal models, although the underlying mechanisms remain unclear. In this study, we investigated whether anagliptin, the dipeptidyl peptidase 4 (DPP-4) inhibitor, attenuates skeletal muscle insulin resistance through endothelial nitric oxide synthase (eNOS) activation in the endothelial cells. We used endothelium-specific Irs2-knockout (ETIrs2KO) mice, which show skeletal muscle insulin resistance resulting from a reduction of insulin-induced skeletal muscle capillary recruitment as a consequence of impaired eNOS activation.In vivo, 8-week-old male ETIrs2KO mice were fed regular chow with or without 0.3% (wt/wt) DPP-4 inhibitor for 8 weeks to assess capillary recruitment and glucose uptake by the skeletal muscle. In vitro, human coronary arterial endothelial cells (HCAECs) were used to explore the effect of glucagon-like peptide 1 (GLP-1) on eNOS activity.Treatment with anagliptin ameliorated the impaired insulin-induced increase in capillary blood volume, interstitial insulin concentration and skeletal muscle glucose uptake in ETIrs2KO mice. This improvement in insulin-induced glucose uptake was almost completely abrogated by the GLP-1 receptor (GLP-1R) antagonist exendin-(9-39). Moreover, the increase in capillary blood volume with anagliptin treatment was also completely inhibited by the NOS inhibitor. GLP-1 augmented eNOS phosphorylation in HCAECs, with the effect completely disappearing after exposure to the protein kinase A (PKA) inhibitor H89. These data suggest that anagliptin treatment enhances insulin-induced capillary recruitment and interstitial insulin concentrations, resulting in improved skeletal muscle glucose uptake by directly acting on the endothelial cells via NO- and GLP-1-dependent mechanisms in vivo.Anagliptin may be a promising agent to ameliorate skeletal muscle insulin resistance in obese patients with type 2 diabetes.

Background As part of the growing lifestyle diversity in modern society, there is wide variation in the time of day individuals choose to exercise. Recent surveys in the US and Japan have reported that on weekdays, more people exercise in the evening, with fewer individuals exercising in the morning or afternoon. Exercise performed in the post-prandial state has little effect on accumulated fat oxidation over 24h (24-h fat oxidation) when energy intake is matched to energy expenditure (energy-balanced condition). The present study explored the possibility that exercise increases 24-h fat oxidation only when performed in a post-absorptive state, i.e. before breakfast. Methods Indirect calorimetry using a metabolic chamber was performed in 10 young, non-obese men over 24h. Subjects remained sedentary (control) or performed 60-min exercise before breakfast (morning), after lunch (afternoon), or after dinner (evening) at 50% of VO 2 max. All trials were designed to be energy balanced over 24h. Time course of energy and substrate balance relative to the start of calorimetry were estimated from the differences between input (meal consumption) and output (oxidation). Findings Fat oxidation over 24h was increased only when exercise was performed before breakfast (control, 456±61; morning, 717±64; afternoon, 446±57; and evening, 432±44kcal/day). Fat oxidation over 24h was negatively correlated with the magnitude of the transient deficit in energy and carbohydrate. Interpretation Under energy-balanced conditions, 24-h fat oxidation was increased by exercise only when performed before breakfast. Transient carbohydrate deficits, i.e., glycogen depletion, observed after morning exercise may have contributed to increased 24-h fat oxidation.

Exercise has numerous health-promoting effects in humans; however, individual responsiveness to exercise with regard to endurance or metabolic health differs markedly. This 'exercise resistance' is considered to be congenital, with no evident acquired causative factors. Here we show that the anti-oxidative hepatokine selenoprotein P (SeP) causes exercise resistance through its muscle receptor low-density lipoprotein receptor-related protein 1 (LRP1). SeP-deficient mice showed a 'super-endurance' phenotype after exercise training, as well as enhanced reactive oxygen species (ROS) production, AMP-activated protein kinase (AMPK) phosphorylation and peroxisome proliferative activated receptor γ coactivator (Ppargc)-1α (also known as PGC-1α; encoded by Ppargc1a) expression in skeletal muscle. Supplementation with the anti-oxidant N-acetylcysteine (NAC) reduced ROS production and the endurance capacity in SeP-deficient mice. SeP treatment impaired hydrogen-peroxide-induced adaptations through LRP1 in cultured myotubes and suppressed exercise-induced AMPK phosphorylation and Ppargc1a gene expression in mouse skeletal muscle-effects which were blunted in mice with a muscle-specific LRP1 deficiency. Furthermore, we found that increased amounts of circulating SeP predicted the ineffectiveness of training on endurance capacity in humans. Our study suggests that inhibitors of the SeP-LRP1 axis may function as exercise-enhancing drugs to treat diseases associated with a sedentary lifestyle.

Pioglitazone (PIO) is widely used as an insulin-sensitizing agent in the treatment of type 2 diabetes, but it also causes an increase in body weight in a dose-dependent manner. Beraprost sodium (BPS), a stable prostaglandin I2 analog, is used clinically for the treatment of peripheral arterial disease and primary pulmonary hypertension. BPS has recently been demonstrated to promote insulin-induced glucose uptake by skeletal muscle. In this study, we examined whether low-dose PIO (PIO-L; 3 mg/kg/day) plus BPS treatment might exert antidiabetic effects without causing body weight gain in obese/diabetic KKAy mice. Treatment with PIO-L plus BPS tended to improve the hepatic insulin resistance and significantly improved the skeletal muscle insulin resistance, yielding a similar degree of hyperglycemia improvement to that obtained with high-dose PIO (PIO-H; 30 mg/kg/day) treatment. Moreover, the increase in body weight observed following PIO-H treatment was not observed following PIO-L plus BPS treatment. An increase in plasma adiponectin levels, which have been shown to be negatively correlated with hepatic glucose production, but not with the glucose disappearance rate during hyperinsulinemic-euglycemic clamp, was observed in the animals treated with PIO-L, PIO-L plus BPS, and PIO-H. This suggests that the improvement in hepatic insulin resistance was associated, at least in part, with an increase in the plasma adiponectin levels observed during PIO treatment. In contrast, treatment with BPS, which failed to increase the plasma adiponectin levels, ameliorated skeletal, but not hepatic insulin resistance. PIO-L plus BPS treatment may represent efficacious treatment for insulin resistance and type 2 diabetes without causing body weight gain.

Purpose Human sleep is generally consolidated into a single prolonged period, and its metabolic consequence is to impose an extended period of fasting. Changes in sleep stage and homeostatic sleep drive following sleep onset may affect sleeping metabolic rate through cross talk between the mechanisms controlling energy metabolism and sleep. The purpose of this study was to isolate the effects of sleep stage and time after sleep onset on sleeping metabolic rate. Methods The sleeping metabolic rate of 29 healthy adults was measured using whole room indirect calorimetry, during which polysomnographic recording of sleep was performed. The effects of sleep stage and time after sleep onset on sleeping metabolic rate were evaluated using a semi-parametric regression analysis. A parametric analysis was used for the effect of sleep stage and a non-parametric analysis was used for the effect of time. Results Energy expenditure differed significantly between sleep stages: wake after sleep onset (WASO) > stage 2, slow wave sleep (SWS), and REM; stage 1 > stage 2 and SWS; and REM > SWS. Similarly, carbohydrate oxidation differed significantly between sleep stages: WASO > stage 2 and SWS; and stage 1 > SWS. Energy expenditure and carbohydrate oxidation decreased during the first half of sleep followed by an increase during the second half of sleep. Conclusions This study identified characteristic phenotypes in energy expenditure and carbohydrate oxidation indicating that sleeping metabolic rate differs between sleep stages.

Indirect calorimetry with a room-size respiratory chamber provides an ideal setting to monitor energy metabolism for a prolonged period. During the last 10 years, experiments with this method have raised interesting observations such as: 1) exercise intensity has no effect on 24 h fat oxidation, 2) exercise has little, if any, effect on 24 h fat oxidation, and 3) exercise before breakfast increases 24 h fat oxidation. To some of the scientific community and general public, the first two statements may be unacceptable. But it can be factually explained that the impact of exercise on energy metabolism is not confined to the period of physical activity itself, and that fat oxidation remains elevated during the post-exercise period. The third observation seems to be insignificant, but contradicts the second one. It is premature to conclude that exercise has no effect on 24 h fat oxidation.

Sodium glucose cotransporter 2 inhibitors have attracted attention as they exert antidiabetic and antiobesity effects. In this study, we investigated the effects of tofogliflozin on glucose homeostasis and its metabolic consequences and clarified the underlying molecular mechanisms. C57BL/6 mice were fed normal chow containing tofogliflozin (0.005%) for 20 weeks or a high-fat diet containing tofogliflozin (0.005%) for 8 weeks ad libitum. In addition, the animals were pair-fed in relation to controls to exclude the influence of increased food intake. Tofogliflozin reduced the body weight gain, mainly because of fat mass reduction associated with a diminished adipocyte size. Glucose tolerance and insulin sensitivity were ameliorated. The serum levels of nonesterified fatty acid and ketone bodies were increased and the respiratory quotient was decreased in the tofogliflozin-treated mice, suggesting the acceleration of lipolysis in the white adipose tissue and hepatic β-oxidation. In fact, the phosphorylation of hormone-sensitive lipase and the adipose triglyceride lipase protein levels in the white adipose tissue as well as the gene expressions related to β-oxidation, such as Cpt1α in the liver, were significantly increased. The hepatic triglyceride contents and the expression levels of lipogenic genes were decreased. Pair-fed mice exhibited almost the same results as mice fed an high-fat diet ad libitum. Moreover, a hyperinsulinemic-euglycemic clamp revealed that tofogliflozin improved insulin resistance by increasing glucose uptake, especially in the skeletal muscle, in pair-fed mice. Taken together, these results suggest tofogliflozin ameliorates insulin resistance and obesity by increasing glucose uptake in skeletal muscle and lipolysis in adipose tissue.

The fatty acid composition of the diet has been linked to the prevalence of diabetes and cardiovascular diseases. Compared with monounsaturated fatty acids, saturated fatty acids decrease fat oxidation and diet-induced thermogenesis. A potential limitation of previous studies was the short duration (≦5h) of calorimetry used. The present study compared the effects of a meal rich in saturated and unsaturated fatty acids on 24-h of fat oxidation. Ten males participated in two sessions of indirect calorimetry in a whole-room metabolic chamber. At each session, subjects consumed three meals rich in palm oil (44.3% as saturated, 42.3% as monounsaturated and 13.4% as polyunsaturated fatty acid) or rapeseed oil (11.7% as saturated, 59.3% as monounsaturated and 29.0% as polyunsaturated fatty acid). Fat oxidation over 24-h was significantly higher in the meal rich in rapeseed oil (779 ± 202 kcal/day) than that rich in palm oil (703 ± 158 kcal/day, P < 0.05), although energy expenditure was similar between both meal conditions. Meal rich in unsaturated fatty acids increased the oxidation of exogenous and/or endogenous fat. The results of a long calorimetry period indicate that rapeseed oil offered an advantage toward increased 24-h fat oxidation in healthy young males.

Whole body fat oxidation increases during exercise. However, 24-h fat oxidation on a day with exercise often remains similar to that of sedentary day, when energy intake is increased to achieve an energy-balanced condition. The present study aimed to examine a possibility that time of the day when exercise is performed makes differences in 24-h fat oxidation. As a potential mechanism of exercise affecting 24-h fat oxidation, its relation to exercise-induced transient energy deficit was examined. Nine young male endurance athletes underwent three trials of indirect calorimetry using a metabolic chamber, in which they performed a session of 100 min of exercise before breakfast (AM), after lunch (PM), or two sessions of 50 min of exercise before breakfast and after lunch (AM/PM) at 65% of maximal oxygen uptake. Experimental meals were designed to achieve individual energy balance. Twenty-four-hour energy expenditure was similar among the trials, but 24-h fat oxidation was 1,142 ± 97, 809 ± 88, and 608 ± 46 kcal/24 h in descending order of its magnitude for AM, AM/PM, and PM, respectively ( P < 0.05). Twenty-four-hour carbohydrate oxidation was 2,558 ± 110, 2,374 ± 114, and 2,062 ± 96 kcal/24 h for PM, AM/PM, and AM, respectively. In spite of energy-balanced condition over 24 h, exercise induced a transient energy deficit, the magnitude of which was negatively correlated with 24-h fat oxidation ( r = −0.72, P < 0.01). Similarly, transient carbohydrate deficit after exercise was negatively correlated with 24-h fat oxidation ( r = −0.40, P < 0.05). The time of the day when exercise is performed affects 24-h fat oxidation, and the transient energy/carbohydrate deficit after exercise is implied as a factor affecting 24-h fat oxidation.

P(論文)

Energy metabolism and substrate oxidation during sleep correlate with sleep stage, suggesting that energy metabolism affects sleep architecture or vice versa. The aim of the present study was to examine whether changes in energy metabolism during sleep, induced by a high-carbohydrate or high-fat meal for dinner, affect sleep architecture. Ten healthy males participated in this study, sleeping 3 nonconsecutive nights in a whole-room calorimeter. The first night was scheduled as an adaptation to the experimental environment. The other 2 nights were experimental calorimetry in a balanced cross-over design with intrasubject comparisons. In each session, subjects comsumed a high carbohydrate (HCD: PFC=10 : 10 : 80) or high fat (HFD: PFC=10 : 78 : 12) meal at 2000 h and slept with a polysomnographic recording in a metabolic chamber for indirect calorimetry (0000 h to 0800 h). Slow wave sleep was decreased during the first sleep cycle and not changed during the second or third sleep cycle under HCD conditions compared with those of HFD. Energy expenditure was not affected by dietary condition but substrate oxidation reflected differences in dietary composition of the dinner during the first and second sleep cycle. The present study suggested the possibility that substrate availability during sleep affects substrate oxidation during sleep, and affects sleep architecture during the first sleep cycle.

Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance. © 2014 by the American Diabetes Association.

The control of sleep/wakefulness is associated with the regulation of energy metabolism. The present experiment was designed to assess the effect of nocturnal blue light exposure on the control of sleep/wakefulness and energy metabolism until next noon.In a balanced cross-over design, nine young male subjects sitting in a room-size metabolic chamber were exposed either to blue LEDs or to no light for 2 h in the evening. Wavelength of monochromatic LEDs was 465 nm and its intensity was 12.1 μW/cm(2).During sleep, sleep architecture and alpha and delta power of EEG were similar in the two experimental conditions. However, the following morning, when subjects were instructed to stay awake in a sitting position, duration judged as sleep at stages 1 and 2 was longer for subjects who received than for those who received no light exposure. Energy metabolism during sleep was not affected by evening blue light exposure, but the next morning energy expenditure, oxygen consumption, carbon dioxide production and the thermic effect of breakfast were significantly lower in subjects who received blue light exposure than in those who received no light exposure.Exposure to low intensity blue light in the evening, which does not affect sleep architecture and energy metabolism during sleep, elicits drowsiness and suppression of energy metabolism the following morning.

Fat oxidation during exercise depends on nutritional state, and exercise performed in the post-absorptive state oxidizes more fat than that performed in the postprandial state. However, the effects of exercise on energy metabolism continue during the post-exercise period, and the difference in fat oxidation during exercise may be compensated for during the post-exercise period. The present study compared the effects of an acute exercise bout in the post-absorptive or postprandial state on 24 h fat oxidation.Twelve young male athletes stayed twice in a room-size metabolic chamber for 24 h indirect calorimetry in a randomized repeated-measure design. Before or after breakfast, i.e. in the post-absorptive or postprandial state, subjects exercised at 50% VO(2)max for 60 min.During the 60 min of exercise, energy expenditure in the two exercise trials were equivalent, but exercise in the post-absorptive state was performed with lower RQ compared with that in the postprandial state (P0.01). The time of exercise relative to breakfast did not affect 24 h energy expenditure (P0.5). However, accumulated 24 h fat oxidation was higher (P0.05) and that of carbohydrate oxidation was lower (P0.05) when exercise was performed in the post-absorptive state.Compared with exercise performed in the postprandial state, exercise performed in the post-absorptive state oxidized more fat and saved more carbohydrate in the body, without affecting 24 h energy expenditure.

Introduction Evening light exposure debilitates the circadian rhythm and elicits sleep disturbance. Blue light peak wavelengths, around 460 nm, suppress melatonin secretion via the non-image-forming system. The effects of nocturnal blue light exposure on sleep have been reported to be specific but rather small (Munch, 2008). This study was designed to assess the effect of nocturnal blue light exposure on sleep and energy metabolism until noon the next day. Materials and methods Nine healthy male volunteers aged between 21 and 25 participated in this study which had a balanced cross-over design with intrasubject comparisons. After 2 h dark adaptation, the subjects were exposed to blue light or no light for 2 h. The peak wavelength of the blue LED was 465 nm, and the horizontal irradiance of the blue light at the height of eye was at 7.02 f EW/cm 2 . Sleep was recorded polysomnographically, and energy metabolism was measured with a whole body indirect calorimeter. Results There were no significant differences in sleep architecture and energy metabolism during the night. However, dozing (stages 1 and 2) was significantly higher (26.0 P 2 consumption, CO 2 production and the thermic effect of food (increase in energy expenditure after breakfast) were significantly lower the following morning in the blue light exposure subjects. Conclusion Contrary to our expectation, sleep architecture and energy metabolism during sleep were not affected by evening exposure to blue light. It might be due to our milder intervention by which subjects in a sitting position did not gaze at the light source set on the ceiling, while the subjects in previous studies directly received brighter light via custom built goggles (Cajochen, 2005; Munch, 2008) or gazed at a light source under the influence of mydriatic agents to dilate pupils (Brainard, 2001). New findings of the present study were that dozing (stages 1 and 2) was significantly increased, and energy metabolism was significantly lower the following morning in blue light exposed subjects. This suggests that modulation of the circadian rhythm is affected by nocturnal blue light exposure and the effect continues in the following daytime even if the intervention was mild. Acknowledgements The present study was supported by a Grant-in-Aid for Scientific Research (No. 23650428). We thank Brian K. Purdue, MECC, University of Tsukuba, for his editorial assistance.