Risk factors analysis of protein energy wasting in children with chronic kidney disease / 中华儿科杂志

Objective: To analyze the clinical characteristics and risk factors of protein energy wasting (PEW) in children with chronic kidney disease (CKD). Methods: Clinical data of 231 children with chronic kidney disease hospitalized in Beijing Children's Hospital affiliated to Capital Medical University from January 2018 to January 2023 were retrospectively analyzed to explore the incidence of PEW. According to the diagnostic criteria of CKDPEW, they were divided into a CKDPEW group and a non PEW group. The comparison between the groups was performed by independent-sample t test and Chi-squared test, and the risk factors were analyzed by multivariate Logistic regression. Results: Among the 231 children, there were 138 males and 93 females, with a visiting age of 9.9 (7.9, 16.0) years; 6 cases were in stage 1, 14 cases in stage 2, 51 cases in stage 3, 36 cases in stage 4, and 124 cases in stage 5. A total of 30 children (13.0%) with CKD PEW were diagnosed at the age of 7. 1 (3.8, 13.2) years, including 1 case in stage 1, 1 case in stage 2, 5 cases in stage 3, 5 cases in stage 4, and 18 cases in stage 5. There were a total of 201 cases (87.0%) in the non PEW group, diagnosed at the age of 11.8 (8.5, 12.2) years, including 5 cases in stage 1, 13 cases in stage 2, 46 cases in stage 3, 31 cases in stage 4, and 106 cases in stage 5. The Chi-squared test and t test showed that the systolic blood pressure, diastolic blood pressure, birth weight and carbon dioxide binding capacity of the CKD PEW group were lower than those of the non PEW group ((109±22) vs. (120±20) mmHg (1 mmHg=0.133 kPa), (72±19) vs. (79±16) mmHg, (2.9±0.5) vs. (3.2±0.6) kg, (17±4) vs. (19±4) mmol/L,t=2.85, 2.14, 0.67, 2.63, all P<0.05). Multivariate logistic regression analysis showed that carbon dioxide binding capacity and birth weight were independent protective factors of CKDPEW in children (OR=0.81 and 0.36, 95%CI=0.73-0.90 and 0.17-0.77, respectively; both P<0.01); the risk of PEW in CKD children decreased by 0.187 times for every 1 mmol/L increment in carbon dioxide binding capacity, and 0.638 times for every 1 kg increment in birth weight. Conclusions: The incidence of protein energy expenditure in children with chronic kidney disease is lower than that in the previous researches. PEW can appear in CKD 1-2 stage, and attention should be paid to it in the early stage of CKD in clinical practice. Low birth weight CKD children are susceptible to PEW, and actively correcting metabolic acidosis can reduce the risk of CKDPEW.

Relationship between Notch signaling pathway and mitochondrial energy metabolism / 中华危重病急救医学

Notch signaling pathway is a highly conserved signaling pathway in the process of evolution. It is composed of three parts: Notch receptor, ligand and effector molecules responsible for intracellular signal transduction. It plays an important role in cell proliferation, differentiation, development, migration, apoptosis and other processes, and has a regulatory effect on tissue homeostasis and homeostasis. Mitochondria are the sites of oxidative metabolism in eukaryotes, where sugars, fats and proteins are finally oxidized to release energy. In recent years, the regulation of Notch signaling pathway on mitochondrial energy metabolism has attracted more and more attention. A large number of data have shown that Notch signaling pathway has a significant effect on mitochondrial energy metabolism, but the relationship between Notch signaling pathway and mitochondrial energy metabolism needs to be specifically and systematically discussed. In this paper, the relationship between Notch signaling pathway and mitochondrial energy metabolism is reviewed, in order to improve the understanding of them and provide new ideas for the treatment of related diseases.

Knockdown of PGC1α suppresses dysplastic oral keratinocytes proliferation through reprogramming energy metabolism / 国际口腔科学杂志·英文版

Oral potentially malignant disorders (OPMDs) are precursors of oral squamous cell carcinoma (OSCC). Deregulated cellular energy metabolism is a critical hallmark of cancer cells. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) plays vital role in mitochondrial energy metabolism. However, the molecular mechanism of PGC1α on OPMDs progression is less unclear. Therefore, we investigated the effects of knockdown PGC1α on human dysplastic oral keratinocytes (DOKs) comprehensively, including cell proliferation, cell cycle, apoptosis, xenograft tumor, mitochondrial DNA (mtDNA), mitochondrial electron transport chain complexes (ETC), reactive oxygen species (ROS), oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and glucose uptake. We found that knockdown PGC1α significantly inhibited the proliferation of DOKs in vitro and tumor growth in vivo, induced S-phase arrest, and suppressed PI3K/Akt signaling pathway without affecting cell apoptosis. Mechanistically, downregulated of PGC1α decreased mtDNA, ETC, and OCR, while enhancing ROS, glucose uptake, ECAR, and glycolysis by regulating lactate dehydrogenase A (LDHA). Moreover, SR18292 (an inhibitor of PGC1α) induced oxidative phosphorylation dysfunction of DOKs and declined DOK xenograft tumor progression. Thus, our work suggests that PGC1α plays a crucial role in cell proliferation by reprograming energy metabolism and interfering with energy metabolism, acting as a potential therapeutic target for OPMDs.

Improving Blood Monocyte Energy Metabolism Enhances Its Ability to Phagocytose Amyloid-β and Prevents Alzheimer's Disease-Type Pathology and Cognitive Deficits / 神经科学通报·英文版

Deficiencies in the clearance of peripheral amyloid β (Aβ) play a crucial role in the progression of Alzheimer's disease (AD). Previous studies have shown that the ability of blood monocytes to phagocytose Aβ is decreased in AD. However, the exact mechanism of Aβ clearance dysfunction in AD monocytes remains unclear. In the present study, we found that blood monocytes in AD mice exhibited decreases in energy metabolism, which was accompanied by cellular senescence, a senescence-associated secretory phenotype, and dysfunctional phagocytosis of Aβ. Improving energy metabolism rejuvenated monocytes and enhanced their ability to phagocytose Aβ in vivo and in vitro. Moreover, enhancing blood monocyte Aβ phagocytosis by improving energy metabolism alleviated brain Aβ deposition and neuroinflammation and eventually improved cognitive function in AD mice. This study reveals a new mechanism of impaired Aβ phagocytosis in monocytes and provides evidence that restoring their energy metabolism may be a novel therapeutic strategy for AD.

Measurement of the Thermic Effect of Food in a Chinese Mixed Diet in Young People / 生物医学与环境科学（英文）

OBJECTIVE@#To determine the thermic effect of food (TEF) in a Chinese mixed diet in young people.@*METHODS@#During the study, the participants were weighed and examined for body composition every morning. The total energy expenditure (TEE) of the participants was measured by the doubly labeled water method for 7 days, and during this period, basal energy expenditure was measured by indirect calorimetry and physical activity energy expenditure was measured by an accelerometer. The value obtained by subtracting basal energy expenditure and physical activity energy expenditure from TEE was used to calculate TEF.@*RESULTS@#Twenty healthy young students (18-30 years; 10 male) participated in the study. The energy intake of the participants was not significantly different from the Chinese Dietary Reference Intake of energy ( P > 0.05). The percentage of energy from protein, fat and carbohydrate were all in the normal range. The intakes of fruits, milk and dietary fiber of the participants were significantly lower than those in the Chinese Dietary Guidelines ( P < 0.05). There was no significant difference in the body weight of the participants during the experiment ( P > 0.05). When adjusted for body weight, there was no significant difference in either TEE or basal energy expenditure between the male and female participants ( P > 0.05). In addition, there was no significant difference in physical activity energy expenditure and TEF between the male and female participants ( P > 0.05). The percentage of TEF in TEE was 8.73%.@*CONCLUSION@#The percentage of TEF in TEE in a Chinese mixed diet in young people was significantly lower than 10% ( P < 0.001). A value of 10% is usually considered to be the TEF in mixed diets as a percentage of TEE.

Comparison of three different measurement methods to determine resting energy expenditure in patients with decompensated hepatitis B cirrhosis / 中华肝脏病杂志

Objective: To compare the differences to determine resting energy expenditure (REE) measured with indirect calorimetry and REE predicted by formula method and body composition analyzer in patients with decompensated hepatitis B cirrhosis, so as to provide theoretical guidance for the implementation of precision nutrition intervention. Methods: Patients with decompensated hepatitis B cirrhosis who were admitted to Henan Provincial People's Hospital from April 2020 to December 2020 were collected. REE was determined by the body composition analyzer and the H-B formula method. Results: were analyzed and compared to REE measured by the metabolic cart. Results A total of 57 cases with liver cirrhosis were included in this study. Among them, 42 were male, aged (47.93 ± 8.62) years, and 15 were female aged (57.20 ± 11.34) years. REE measured value in males was (1 808.14 ± 201.47) kcal/d, compared with the results calculated by the H-B formula method and the measured result of body composition, and the difference was statistically significant (P = 0.002 and 0.003, respectively). REE measured value in females was (1 496.60 ± 131.28) kcal/d, compared with the results calculated by the H-B formula method and the measured result of body composition, and the difference was statistically significant (P = 0.016 and 0.004, respectively). REE measured with the metabolic cart had correlation with age and area of visceral fat in men (P = 0.021) and women (P = 0.037). Conclusion: Metabolic cart use will be more accurate to obtain resting energy expenditure in patients with decompensated hepatitis B cirrhosis. Body composition analyzer and formula method may underestimate REE predictions. Simultaneously, it is suggested that the effect of age on REE in H-B formula should be fully considered for male patients, while the area of visceral fat may have a certain impact on the interpretation of REE in female patients.

Excess Oxygen Supply for Different Time Periods Affect Energy Metabolism in Rat Alveolar Epithelial Type Ⅱ Cells / 中国医学科学院学报

Objective To observe the effect of excess oxygen supply for different time periods on the mitochondrial energy metabolism in alveolar epithelial type Ⅱ cells. Methods Rat RLE-6TN cells were assigned into a control group (21% O2 for 4 h) and excess oxygen supply groups (95% O2 for 1,2,3,and 4 h,res-pectively).The content of adenosine triphosphate (ATP),the activity of mitochondrial respiratory chain complex V,and the mitochondrial membrane potential were determined by luciferase assay,micro-assay,and fluorescent probe JC-1,respectively.Real-time fluorescence quantitative PCR was employed to determine the mRNA levels of NADH dehydrogenase subunit 1 (ND1),cytochrome b (Cytb),cytochrome C oxidase subunit I (COXI),and adenosine triphosphatase 6 (ATPase6) in the core subunits of mitochondrial respiratory chain complexes Ⅰ,Ⅲ,Ⅳ,and Ⅴ,respectively. Results Compared with the control group,excess oxygen supply for 1,2,3,and 4 h down-regulated the mRNA levels of ND1 (q=24.800,P<0.001;q=13.650,P<0.001;q=9.869,P<0.001;q=20.700,P<0.001),COXI (q=16.750,P<0.001;q=10.120,P<0.001;q=8.476,P<0.001;q=14.060,P<0.001),and ATPase6 (q=22.770,P<0.001;q=15.540,P<0.001;q=12.870,P<0.001;q=18.160,P<0.001).Moreover,excess oxygen supply for 1 h and 4 h decreased the ATPase activity (q=9.435,P<0.001;q=11.230,P<0.001) and ATP content (q=5.615,P=0.007;q=5.029,P=0.005).The excess oxygen supply for 2 h and 3 h did not cause significant changes in ATPase activity (q=0.156,P=0.914;q=3.197,P=0.116) and ATP content (q=0.859,P=0.557;q=1.273,P=0.652).There was no significant difference in mitochondrial membrane potential among the groups (F=0.303,P=0.869). Conclusion Short-term excess oxygen supply down-regulates the expression of the core subunits of mitochondrial respiratory chain complexes and reduces the activity of ATPase,leading to the energy metabolism disorder of alveolar epithelial type Ⅱ cells.

Effects and mechanism of p53 gene deletion on energy metabolism during the pluripotent transformation of spermatogonial stem cells / 生理学报

Previous studies have shown that long-term spermatogonial stem cells (SSCs) have the potential to spontaneously transform into pluripotent stem cells, which is speculated to be related to the tumorigenesis of testicular germ cells, especially when p53 is deficient in SSCs which shows a significant increase in the spontaneous transformation efficiency. Energy metabolism has been proved to be strongly associated with the maintenance and acquisition of pluripotency. Recently, we compared the difference in chromatin accessibility and gene expression profiles between wild-type (p53+/+) and p53 deficient (p53-/-) mouse SSCs using the Assay for Targeting Accessible-Chromatin with high-throughput sequencing (ATAC-seq) and transcriptome sequencing (RNA-seq) techniques, and revealed that SMAD3 is a key transcription factor in the transformation of SSCs into pluripotent cells. In addition, we also observed significant changes in the expression levels of many genes related to energy metabolism after p53 deletion. To further reveal the role of p53 in the regulation of pluripotency and energy metabolism, this paper explored the effects and mechanism of p53 deletion on energy metabolism during the pluripotent transformation of SSCs. The results of ATAC-seq and RNA-seq from p53+/+ and p53-/- SSCs revealed that gene chromatin accessibility related to positive regulation of glycolysis and electron transfer and ATP synthesis was increased, and the transcription levels of genes encoding key glycolytic enzymes and regulating electron transport-related enzymes were markedly increased. Furthermore, transcription factors SMAD3 and SMAD4 promoted glycolysis and energy homeostasis by binding to the chromatin of the Prkag2 gene which encodes the AMPK subunit. These results suggest that p53 deficiency activates the key enzyme genes of glycolysis in SSCs and enhances the chromatin accessibility of genes associated with glycolysis activation to improve glycolysis activity and promote transformation to pluripotency. Moreover, SMAD3/SMAD4-mediated transcription of the Prkag2 gene ensures the energy demand of cells in the process of pluripotency transformation and maintains cell energy homeostasis by promoting AMPK activity. These results shed light on the importance of the crosstalk between energy metabolism and stem cell pluripotency transformation, which might be helpful for clinical research of gonadal tumors.

Therapeutic potential of alkaloid extract from Codonopsis Radix in alleviating hepatic lipid accumulation: insights into mitochondrial energy metabolism and endoplasmic reticulum stress regulation in NAFLD mice / 中国天然药物

Alkaloids are a class of naturally occurring bioactive compounds that are widely distributed in various food sources and Traditional Chinese Medicine. This study aimed to investigate the therapeutic effects and underlying mechanisms of alkaloid extract from Codonopsis Radix (ACR) in ameliorating hepatic lipid accumulation in a mouse model of non-alcoholic fatty liver disease (NAFLD) induced by a high-fat diet (HFD). The results revealed that ACR treatment effectively mitigated the abnormal weight gain and hepatic injury associated with HFD. Furthermore, ACR ameliorated the dysregulated lipid metabolism in NAFLD mice, as evidenced by reductions in serum triglyceride, total cholesterol, and low-density lipoprotein levels, accompanied by a concomitant increase in the high-density lipoprotein level. ACR treatment also demonstrated a profound anti-oxidative effect, effectively alleviating HFD-induced oxidative stress and promoting ATP production. These effects were achieved through the up-regulation of the activities of mitochondrial electron transfer chain complexes I, II, IV, and V, in addition to the activation of the AMPK/PGC-1α pathway, suggesting that ACR exhibits therapeutic potential in alleviating the HFD-induced dysregulation of mitochondrial energy metabolism. Moreover, ACR administration mitigated HFD-induced endoplasmic reticulum (ER) stress and suppressed the overexpression of ubiquitin-specific protease 14 (USP14) in NAFLD mice. In summary, the present study provides compelling evidence supporting the hepatoprotective role of ACR in alleviating lipid deposition in NAFLD by improving energy metabolism and reducing oxidative stress and ER stress. These findings warrant further investigation and merit the development of ACR as a potential therapeutic agent for NAFLD.

Potential implications of ketone body metabolism changes and ketogenic therapy in the treatment of heart failure / 中华危重病急救医学

Heart failure (HF) has become a major challenge in the treatment of global cardiovascular diseases. Great progress has been made in the drug treatment of HF, however, rehospitalization rate and mortality of patients with HF are still high. Hence, there is an urgent need to explore new treatment strategy and new underlying pathogenic mechanisms. In recent years, some researchers have suggested that regulation of ketone body metabolism may become a potentially promising therapeutic approach for HF. Some studies showed that the oxidative utilization of fatty acids and glucose was decreased in the failing heart, accompanied by the increase of ketone body oxidative metabolism. The enhancement of ketone body metabolism in HF is a compensatory change during HF. The failing heart preferentially uses ketone body oxidation to provide energy, which helps to improve the body's cardiac function. This review will discuss the potential significance of ketone body metabolism in the treatment of HF from three aspects: normal myocardial ketone body metabolism, the change of ketone body metabolism in HF, the effect of ketogenic therapy on HF and its treatment.

Andrographolide protects against atrial fibrillation by alleviating oxidative stress injury and promoting impaired mitochondrial bioenergetics / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia seen in clinical settings, which has been associated with substantial rates of mortality and morbidity. However, clinically available drugs have limited efficacy and adverse effects. We aimed to investigate the mechanisms of action of andrographolide (Andr) with respect to AF. We used network pharmacology approaches to investigate the possible therapeutic effect of Andr. To define the role of Andr in AF, HL-1 cells were pro-treated with Andr for 1 h before rapid electronic stimulation (RES) and rabbits were pro-treated for 1 d before rapid atrial pacing (RAP). Apoptosis, myofibril degradation, oxidative stress, and inflammation were determined. RNA sequencing (RNA-seq) was performed to investigate the relevant mechanism. Andr treatment attenuated RAP-induced atrial electrophysiological changes, inflammation, oxidative damage, and apoptosis both in vivo and in vitro. RNA-seq indicated that oxidative phosphorylation played an important role. Transmission electron microscopy and adenosine triphosphate (ATP) content assay respectively validated the morphological and functional changes in mitochondria. The translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus and the molecular docking suggested that Andr might exert a therapeutic effect by influencing the Keap1-Nrf2 complex. In conclusions, this study revealed that Andr is a potential preventive therapeutic drug toward AF via activating the translocation of Nrf2 to the nucleus and the upregulation of heme oxygenase-1 (HO-1) to promote mitochondrial bioenergetics.

Investigation of tactile gait parameters based on deep learning of energy consumption estimation algorithm in sport / Investigação sobre parâmetros tácteis de marcha baseados no aprendizado profundo do algoritmo de estimativa de consumo energético no esporte / Investigación sobre los parámetros táctiles de marcha basados en el aprendizaje profundo del algoritmo de estimación del consumo de energía en el deporte

ABSTRACT Introduction In medicine, Deep Learning is a type of machine learning that aims to train computers to perform human tasks by simulating the human brain. Gait recognition and gait motion simulation is one of the most interesting research areas in the field of biometrics and can benefit from this technological feature. Objective To use Deep Learning to format and validate according to the dynamic characteristics of gait. Methods Gait was used for identity recognition, and gait recognition based on kinematics and dynamic gait parameters was performed through pattern recognition, including the position and the intensity value of maximum pressure points, pressure center point, and pressure ratio. Results The investigation shows that the energy consumption of gait as modeled analyzed, and the model of gait energy consumption can be obtained, which is comprehensively affected by motion parameters and individual feature parameters. Conclusion Real-time energy measurement is obtained when most people walk. The research shows that the gait frequency and body parameters obtained from the tactile parameters of gait biomechanics can more accurately estimate the energy metabolism of exercise and obtain the metabolic formula of exercise. There is a good application prospect for assessing energy metabolism through the tactile parameters of gait. Level of evidence II; Therapeutic studies - investigating treatment outcomes.

RESUMO Introdução Na medicina, o aprendizado profundo é um tipo de aprendizado de máquina que visa treinar computadores para a realização de tarefas humanas simulando o cérebro humano. O reconhecimento da marcha e a simulação do movimento de marcha são um dos pontos de maior interesse da investigação no campo da biometria e pode ser beneficiado com esse recurso tecnológico. Objetivo Utilizar o aprendizado profundo para formatar e validar, de acordo com as características dinâmicas da marcha. Métodos A marcha foi utilizada para o reconhecimento da identidade, e o reconhecimento da marcha baseado na cinemática e parâmetros dinâmicos de marcha foi realizado através do reconhecimento de padrões, incluindo a posição e o valor de intensidade dos pontos de pressão máxima, ponto central de pressão e relação de pressão. Resultados A investigação mostra que o consumo de energia da marcha como modelado analisado, e o modelo de consumo de energia da marcha pode ser obtido, o qual é afetado de forma abrangente pelos parâmetros de movimento e pelos parâmetros de características individuais. Conclusão A medição de energia em tempo real é obtida quando a maioria das pessoas caminha. A investigação mostra que a frequência da marcha e os parâmetros corporais obtidos a partir dos parâmetros tácteis da biomecânica da marcha podem estimar com maior precisão o metabolismo energético do exercício e obter a fórmula metabólica do exercício. Há uma boa perspectiva de aplicação para avaliar o metabolismo energético através dos parâmetros tácteis da marcha. Nível de evidência II; Estudos terapêuticos - investigação dos resultados do tratamento.

RESUMEN Introducción En medicina, el aprendizaje profundo es un tipo de aprendizaje que pretende entrenar a los ordenadores para que realicen tareas humanas simulando el cerebro humano. El reconocimiento de la marcha y la simulación de su movimiento es uno de los puntos más interesantes de la investigación en el campo de la biometría y puede beneficiarse de este recurso tecnológico. Objetivo Utilizar el aprendizaje profundo para formatear y validar según las características dinámicas de la marcha. Métodos Se utilizó la marcha para el reconocimiento de la identidad, y el reconocimiento de la marcha basado en la cinemática y los parámetros dinámicos de la marcha se realizó mediante el reconocimiento de patrones, incluyendo la posición y el valor de la intensidad de los puntos de presión máxima, el punto de presión central y la relación de presión. Resultados La investigación muestra que el consumo de energía de la marcha, tal y como se analizó, y el modelo de consumo de energía de la marcha se puede obtener, que es ampliamente afectado por los parámetros de movimiento y los parámetros de las características individuales. Conclusión La medición de la energía en tiempo real se obtiene cuando la mayoría de la gente camina. La investigación muestra que la frecuencia de la marcha y los parámetros corporales obtenidos a partir de los parámetros táctiles de la biomecánica de la marcha pueden estimar con mayor precisión el metabolismo energético del ejercicio y obtener la fórmula metabólica del mismo. Existe una buena perspectiva de aplicación para evaluar el metabolismo energético a través de los parámetros táctiles de la marcha. Nivel de evidencia II; Estudios terapéuticos - investigación de los resultados del tratamiento.

Sintomatología depresiva y relación con la actividad física en estudiantes de una universidad con enfoque deportivo / Depressive symptomatology and its relationship to physical activity in students from sport-oriented universities

Introducción: La depresión es una problemática de salud pública responsable de alta carga de mortalidad, afecta principalmente a jóvenes universitarios. La evidencia sugiere que la participación en actividad física genera beneficios en salud mental. Resulta importante estudiar esta asociación teniendo en cuenta otra serie de factores como variables sociodemográficas y el tipo de carrera universitaria. Objetivo: Estimar la prevalencia de sintomatología depresiva y evaluar si el nivel de actividad física podría ser un factor protector en estudiantes de una universidad con enfoque deportivo. Materiales y métodos: Estudio transversal con muestra representativa de 291 estudiantes. Se aplicó cuestionario Beck II y versión larga del International Physical Activity Questionnaire (IPAQ). Se realizó análisis univariado y bivariado con razones de prevalencia para depresión, según nivel de actividad física ajustadas mediante modelos de regresión generalizados con vínculo logarítmico de distribución binomial. Resultados: Las prevalencias de síntomas de depresión e inactividad física son respectivamente 27% y 22%. La prevalencia de síntomas de depresión es 46% mayor en quienes no son suficientemente activos (RP: 1,46 IC95%:0,95-2,25). Conclusiones: La prevalencia de síntomas de depresión e inactividad física más bajas comparadas con poblaciones similares, probablemente se relacionan con el enfoque deportivo de la institución.

Introduction: Depression is a public health problem that has a burden of high mortality, mainly affecting the young university student population. The evidence suggests that participation in physical activity generates mental health benefits. It is important to study this association as well as the relationship between depression and sociodemographic variables and university program. Objective: To estimate the prevalence of depressive symptomatology and assess whether physical activity levels can be a Protective factor in university students enrolled in sports programs. Materials and methods: Cross-sectional study with a representative sample of 291 students. The Beck II questionnaire and long version of the International Physical Activity Questionnaire (IPAQ) were applied. Univariate and bivariate analyses were performed with prevalence ratios for depression, according to the level of physical activity adjusted by generalized regression models with logarithmic link of binomial distribution. Results: The prevalence rates of depression symptoms and physical inactivity were 27% and 22%, respectively. The prevalence of depression symptoms is 46% higher in those who are not sufficiently active (RP: 1.46 IC95%:0.95-2.25). Conclusions: Prevalence of depressive symptoms and physical inactivity were lower compared to similar populations and are probably related to the sport focus of the institution.

Microbiota intestinal y modulación del tejido adiposo en la patogénesis de la obesidad / Gut microbiota and modulation of adipose tissue in the pathogenesis of obesity

Las investigaciones realizadas durante el último siglo relacionadas con la descripción de la Microbiota Intestinal (MI) sugieren una relación concreta entre su composición y la salud del huésped. Su desregulación denominada disbiosis intestinal ha sido asociada a distintos tipos de enfermedades gastrointestinales, metabólicas, oncológicas e incluso psiquiátricas. Destacan numerosos reportes que han informado la condición de disbiosis en la obesidad, tanto en modelos animales como humanos de distintos grupos etarios y regiones del mundo. A su vez, la composición del microbioma también ha logrado asociarse a las diferentes comorbilidades de la obesidad, postulando que la MI posee influencia en la disfunción del tejido adiposo (TA), entendiendo que corresponde al principal modulador de la patogénesis de la obesidad. Sin embargo, aún no es posible establecer una explicación mecanicista plausible. Actualmente, la utilización de tecnologías multiómicas, junto con la evaluación de variables fisiológicas, nos podrían proporcionar una mejor comprensión a la incógnita planteada. Frente a esto, el presente trabajo tiene como objetivo revisar los últimos avances en la comprensión de la influencia de la microbiota intestinal en el TA y su contribución a los mecanismos relacionados con la patogénesis de la obesidad. Entre los principales mecanismos identificados, la evidencia reporta nexos fisiológicos entre la composición de la MI y la modulación de inflamación, permeabilidad intestinal y adipogénesis. Las vías implicadas derivan de la influencia de la disbiosis intestinal en el accionar de ácidos grasos de cadena corta, claudinas, macrófagos, oligosacáridos, entre otros. Los mecanismos implicados, principalmente estudiados en modelos animales, deberían ser considerados para su evaluación en próximos estudios longitudinales y experimentales en humanos con el fin de obtener una mayor comprensión sobre la implicancia de cada mecanismo en la patogenia global de la obesidad(AU)

The investigations carried out during the last century related to the description of the Gut Microbiota (GM) suggest a concrete relationship between its composition and the health of the host. Its deregulation called intestinal dysbiosis has been associated with different types of gastrointestinal, metabolic, oncological and even psychiatric diseases. Numerous reports that have described the condition of dysbiosis in obesity stand out, both in animal and human models of different age groups and regions of the world. In turn, the composition of the microbiome has also been associated with the different comorbidities of obesity, postulating that MI has an influence on adipose tissue (AT) dysfunction, understanding that it corresponds to the main modulator of the pathogenesis of obesity. However, it is not yet possible to establish a plausible mechanistic explanation. Currently, the use of multi-omics technologies, together with the evaluation of physiological variables, could provide us with a better understanding of the question raised. In view of this, this review aims to review the latest advances in understanding the influence of the intestinal microbiota on AT and its contribution to the mechanisms related to the pathogenesis of obesity. Among the main mechanisms identified, the evidence reports physiological links between the composition of GM and the modulation of inflammation, intestinal permeability and adipogenesis. The pathways involved derive from the influence of intestinal dysbiosis on the action of short-chain fatty acids, claudins, macrophages, oligosaccharides, among others. The mechanisms involved, mainly studied in animal models, should be considered for evaluation in future longitudinal and experimental studies in humans in order to obtain a better understanding of the implication of each mechanism in the global pathogenesis of obesity(AU)

Estimación del gasto energético y tiempo dedicado a la actividad física en escolares costarricenses con sobrepeso u obesidad por medio del acelerómetro Actiheart / Energy expenditure and time spent on physical activity in Costa Rican schoolchildren with overweight or obesity by means of the Actiheart accelerometer

Resumen Objetivo: determinar el gasto energético y el tiempo dedicado a actividad física en condición de vida libre de escolares costarricenses con sobrepeso u obesidad. Metodología: participaron 31 niños y 13 niñas entre 6 y 9 años (7.6 ± 1.03 años) con sobrepeso u obesidad, estado nutricional que se estableció según el IMC. Las variables del estudio fueron la antropometría, el porcentaje de grasa corporal (%GC), el gasto energético total producto de la actividad física a lo largo del día (GEAF total diario), el gasto energético por actividad física (GEAF) y el tiempo dedicado a la actividad física (TAF), las dos últimas se estimaron según condición sedentaria, ligera, moderada o vigorosa, por medio del acelerómetro Actiheart. Resultados: la talla y el %GC fueron significativamente mayores en las niñas (126.8 ± 5.9 cm, 34.0 ± 6.4 %GC) que en los niños (123.0 ± 5.4 cm, 25.2 ± 6.9 %GC). Los niños registraron un GEAF total diario de 824 ± 228.1 kcal/day, GEAF moderada + vigorosa de 285.6 ± 131.7 kcal/day y un TAF moderada + vigorosa de 147.0 ± 66.6 min, valores superiores (p<0.05) a los de las niñas 395 ± 144.4 kcal/day, 139.6 ± 90.1 kcal/day y 75.6 ± 43.2 min, respectivamente. Conclusiones: los escolares cumplen más de los 60 min/día recomendados de TAF de moderada a vigorosa intensidad, sin embargo, el GEAF de moderada a vigorosa intensidad no alcanza el mínimo de 300 kcal/día para la reducción de peso, lo cual podría ser una de las causas del sobrepeso.

Abstract Objective: To determine the energy expenditure and time spent on physical activities in Costa Rican overweight or obese schoolchildren in free-living conditions. Methodology: Participants were 31 boys and 13 girls aged 6 to 9 years old (7.6 ± 1.03 years) with overweight or obesity; nutritional status was established by BMI. The variables of the study were: anthropometric, body fat percentage (%BF), total energy expenditure product of physical activity performed during the day (EEPA daily total), plus the energy expenditure by physical activity (EEPA), and time spent on physical activity (TPA), both variables in sedentary condition, light, moderate and vigorous intensity estimated by the Actiheart accelerometer. Results: Size and %BF were significantly higher in girls (126.8 ± 5.9 cm, 34.0 ± 6.4% BF) than in boys (123.0 ± 5.4 cm, 25.2 ± 6.9% BF). Boys recorded a daily total EEPA of 824 ± 228.1 kcal / day, moderate + vigorous EEPA 285.6 ± 131.7 kcal / day and a moderate + vigorous TPA 147.0 ± 66.6 min; significantly higher (P <0.05) than girls 395 ± 144.4 kcal / day, 139.6 ± 90.1 kcal / day and 75.6 ± 43.2 min respectively . Conclusions: Schoolchildren perform over 60 min/day moderate to vigorous intensity PA recommended, however; the EEPA moderate to vigorous intensity does not meet the minimum recommendation of 300 kcal / day for weight reduction. This could be one of the causes for overweight schoolchildren.

Markers of mitochondrial energy metabolism and their potential relationships with fatigue in human adults: a scoping review

This scoping review aimed to synthesize the best available evidence of the associations between molecular and genetic markers of mitochondrial metabolism and fatigue in human adults. The research question guiding this review was, "Are there potential relationships between mitochondrial metabolism markers and fatigue?" The literature search used three terms (mitochondria; fatigue; energy metabolism), which yielded 263 manuscripts and 22 theses/dissertations. The studies included in the review had to meet three criteria: (1) Include adult participants (≥18 years of age); (2) Show a relationship between mitochondrial energy metabolism and fatigue; (3) Be published in English, Spanish, or Portuguese. Of the 17 articles included for a full-text review, some had a cross-sectional design (6/17, 35%), and more than half (12/17, 70%) were published between 2015 and 2020. The predominant population studied were patients diagnosed with chronic fatigue syndrome (9/17, 53%). Most studies (15/17, 88%) assessed fatigue with validated instruments. Mitochondrial markers associated with fatigue are a) mitochondrial transport pathways and respiratory chain, b) mutations in mitochondrial DNA, and c) energy disorders in cells of the immune system, such as natural killer cells. Mitochondrial metabolic activities, such as the production and transport of ATP, are significant components that may help understand the etiology of fatigue. Future directions should include longitudinal study designs, characterization of fatigue phenotypes, and the identification of markers involved in production and transport pathways. The clinical relevance in this field can lead to interventions targeting mitochondrial markers to reduce or prevent fatigue.

Mitochondrial energy metabolism in baby hamster kidney (BHK-21/C13) cells treated with karnozin extra® / Metabolismo energético mitocondrial en células de riñón de hámster bebé (BHK-21 / C13) tratadas con karnozin extra®

SUMMARY: Carnosine is known as a natural dipeptide, which inhibits the proliferation of tumor cells throughout its action on mitochondrial respiration and cell glycolysis. However, not much is known about its effects on the metabolism of healthy cells. We explored the effects of Karnozin EXTRA® capsule with different concentrations of L-carnosine, on the cell viability and the expressions of intermediate filament vimentin (VIM) and superoxide dismutase (SOD2) in normal fibroblasts BHK-21/C13. Furthermore, we investigated its action on the energy production of these cells. Cell viability was quantified by the MTT assay. The Clark oxygen electrode (Oxygraph, Hansatech Instruments, England) was used to measure the "intact cell respiration rate", state 3 of ADP-stimulated oxidation, maximum oxidation capacity and the activities of complexes I, II and IV. Results showed that Karnozin EXTRA® capsule in concentrations of 2 and 5 mM of L-carnosine did not induce toxic effects and morphological changes in treated cells. Our data revealed a dose-dependent immunofluorescent signal amplification of VIM and SOD2 in the BHK-21/C13 cell line. This supplement substantially increased the recorded mitochondrial respiration rates in the examined cell line. Due to the stimulation of mitochondrial energy production in normal fibroblasts, our results suggested that Karnozin EXTRA® is a potentially protective dietary supplement in the prevention of diseases with altered mitochondrial function.

RESUMEN: La carnosina se conoce como dipéptido natural, que inhibe la proliferación de células tumorales a través de su acción sobre la respiración mitocondrial y la glucólisis celular. Sin embargo, no se sabe mucho de sus efectos sobre el metabolismo de las células sanas. Exploramos los efectos de la cápsula Karnozin EXTRA® con diferentes concentraciones de L-carnosina, sobre la viabilidad celular y las expresiones de vimentina de filamento intermedio (VIM) y superóxido dismutasa (SOD2) en fibroblastos normales BHK-21 / C13. Además, estudiamos su acción sobre la producción de energía de estas células. La viabilidad celular se cuantificó mediante el ensayo MTT. Se utilizó el electrodo de oxígeno Clark (Oxygraph, Hansatech Instruments, Inglaterra) para medir la "tasa de respiración de células intactas", el estado 3 de oxidación estimulada por ADP, la capacidad máxima de oxidación y las actividades de los complejos I, II y IV. Los resultados mostraron que la cápsula de Karnozin EXTRA® en concentraciones de 2 y 5 mM de L- carnosina no indujo efectos tóxicos ni cambios morfológicos en las células tratadas. Nuestros datos revelaron una amplificación de señal inmunofluorescente dependiente de la dosis de VIM y SOD2 en la línea celular BHK-21 / C13. Este suplemento aumentó sustancialmente las tasas de respiración mitocondrial registradas en la línea celular examinada. Debido a la estimulación de la producción de energía mitocondrial en fibroblastos normales, nuestros resultados sugirieron que Karnozin EXTRA® es un suplemento dietético potencialmente protector en la prevención de enfermedades con función mitocondrial alterada.

The hypothalamus for whole-body physiology: from metabolism to aging

Obesity and aging are two important epidemic factors for metabolic syndrome and many other health issues, which contribute to devastating diseases such as cardiovascular diseases, stroke and cancers. The brain plays a central role in controlling metabolic physiology in that it integrates information from other metabolic organs, sends regulatory projections and orchestrates the whole-body function. Emerging studies suggest that brain dysfunction in sensing various internal cues or processing external cues may have profound effects on metabolic and other physiological functions. This review highlights brain dysfunction linked to genetic mutations, sex, brain inflammation, microbiota, stress as causes for whole-body pathophysiology, arguing brain dysfunction as a root cause for the epidemic of aging and obesity-related disorders. We also speculate key issues that need to be addressed on how to reveal relevant brain dysfunction that underlines the development of these disorders and diseases in order to develop new treatment strategies against these health problems.

Yixin Ningshen Tablet Alleviates Comorbidity of Myocardial Infarction and Depression by Enhancing Myocardial Energy Metabolism and Increasing Availability of Monoamine Neurotransmitter / 中国结合医学杂志

OBJECTIVE@#To investigate the therapeutic effect of Yixin Ningshen Tablet (YXNS) on comorbidity of myocardial infarction (MI) and depression in rats and explore the underlying mechanism.@*METHODS@#The Sprague-Dawley rats were randomly divided into 5 groups with 7 rats in each group according to their weights, including control, model, fluoxetine (FLXT, 10 mg/kg), low-dose YXNS (LYXNS, 100 mg/kg), and high-dose YXNS (HYXNS, 300 mg/kg) groups. All rats were pretreated with corresponding drugs for 12 weeks. The rat model of MI and depression was constructed by ligation of left anterior descending coronary artery and chronic mild stress stimulation. The echocardiography, sucrose preference test, open field test, and forced swim test were performed. Myocardial infarction (MI) area and myocardial apoptosis was also detected. Serum levels of interleukin (IL)-6, IL-1β, tumor necrosis factor-α (TNF-α), 5-hydroxytryptamine (5-HT), adrenocorticotrophic hormone (ACTH), corticosterone (CORT), and norepinephrine (NE) were determined by enzyme linked immunosorbent assay. The proteins of adenosine 5'-monophosphate -activated protein kinase (AMPK), p-AMPK, peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), and nuclear respiratory factor 1 (NRF1) in heart were detected by Western blot analysis. The expression levels of TNF-α, IL-6, indoleamine 2,3-dioxygenase (IDO1), kynurenine 3-monooxygenase (KMO), and kynureninase (KYNU) in hippocampus were detected by real-time quantitative polymerase chain reaction.@*RESULTS@#Compared with the model group, the cardiac function of rats treated with YXNS improved significantly (P<0.01). Meanwhile, YXNS effectively reduced MI size and cardiomyocytes apoptosis of rats (P<0.01 or P<0.05), promoted AMPK phosphorylation, and increased PGC-1α protein expression (P<0.01 or P<0.05). HYXNS significantly increased locomotor activity of rats, decreased the levels of TNF-α, IL-6 and IL-1β, and increased the serum levels of 5-HT, NE, ACTH, and CORT (all P<0.05). Moreover, HYXNS decreased the mRNA expressions of IDO1, KMO and KYNU (P<0.05).@*CONCLUSIONS@#YXNS can relieve MI by enhancing myocardial energy metabolism. Meanwhile, YXNS can alleviate depression by resisting inflammation and increasing availability of monoamine neurotransmitters. It may be used as a potential drug to treat comorbidity of MI and depression.

Simulation Study on the Influence of Sampling Delay on the Accuracy of Energy Metabolism Measurement / 中国医疗器械杂志

Indirect energy metabolism measurement is the gold standard for providing nutritional support for critical illness. The accuracy of the measurement data directly affects the outcome of the disease. In order to study the influence of sampling delay on the accuracy of energy metabolism measurement under mechanical ventilation, the Matlab/Simulink platform and respiratory electrical model were used for simulation and quantitative analysis. The results show that the error of indirect energy metabolism measurement increases with the increase of sampling delay, the error of sampling delay in mechanical ventilation mode is larger than that of spontaneous breathing, and the error of sampling delay in PCV mode of mechanical ventilation is larger than that in VCV mode. Therefore, there should be different sampling delay compensation strategies under severe mechanical ventilation and its different control modes.