Efectos del Ramadán como forma de ayuno sobre el rendimiento deportivo

Fundamento: El Ramadán, es un tipo de ayuno religioso muy extendido entre la población deportista tanto a nivel popular como a nivel profesional. Esta práctica puede suponer un “hándicap” para los deportistas, especialmente los de más alto nivel, ya que hay estudios que afirman que podría tratarse de una práctica perjudicial para su rendimiento deportivo. Por esta razón, es pertinente analizar los posibles efectos que puede tener esta práctica sobre las capacidades aeróbicas y anaeróbicas y las posibles modificaciones que podrían dar pie a minimizar este posible efecto deletéreo. En base a esto, el objetivo de esta revisión sistemática es analizar la evidencia existente sobre los posibles efectos del Ramadán sobre el rendimiento deportivo. Metodología: Se realizó una revisión sistemática utilizando la base de datos PubMed como principal buscador. La revisión siguió la metodología Prisma, y los términos utilizados para dicha revisión fueron: Effects of Ramadán AND performance. Resultados: Se obtuvieron un total de 18 artículos que analizaban los efectos del Ramadán sobre distintas variables del rendimiento deportivo en atletas aficionados y profesionales. El resultado obtenido en general es controvertido. A día de hoy no está claro si los efectos del Ramadán sobre los deportistas son significativos como para traducirse en un menor rendimiento físico. Conclusión: Por un lado, podría existir cierto efecto del Ramadán sobre el rendimiento deportivo, especialmente sobre el aeróbico. No obstante, esto aún no está claro. Por esta razón son necesarios más estudios que decanten la balanza hacia uno u otro lado. No obstante, es conveniente optimizar el entorno que rodea a este tipo de ayuno, para que, en el caso de tener algún efecto perjudicial, este sea mínimo. Especialmente cuando se trata de deportistas de alto nivel en los que un pequeño efecto puede resultar decisivo.Background: Ramadan fasting is very widespread between professional and amateur athletes. This kind of fasting could have a detrimental effect over sport performance. This is the reason why it could be very interesting to analyze the potential negative effects that this could have over the sport performance. Even more if we take into account the impact that could have even a very small effect among professional or high-level athletes. For this reason, it is relevant to review the present knowledge available in terms of the effect of the Ramadan fasting over the aerobic and the anaerobic capacities and the possible strategies to minimize the yet controversial negative effect. For this reason, the aim of this systematic review is to analyze the available evidence about the potential detrimental effects of the Ramadan fasting over the sports performance. Methodology: A systematic review was performed using the PubMed database as the main searching tool. The review used the Prisma methodology, and the key word used for the research were: Effects of Ramadan AND performance. Results: A total of 18 articles were included in the systematic review. They analyzed the effect of Ramadan fasting on different variables of sport performance in amateur and professional athletes. The overall results are controversial. It is not clear that the effects of the Ramadan fasting are enough to translate into a lower physical performance. Conclusion: On the one hand, there could be some negative effect of Ramadan on sport performance, especially aerobic performance. However, this is unclear and more studies are needed to explain the role Ramadan could have over athlete’s performance. However, it is convenient to optimize the environment that surrounds this practice in case there is little effect. Even more if we are dealing with professional athletes

Tratamiento y prevención de las enfermedades cardiovasculares: efecto de los ácidos grasos omega 3 frente a la hipoxia

La cardiopatía isquémica y el accidente cerebrovascular se presentan como las primeras causas de muerte a nivel mundial. El desarrollo de ambas está condicionado por múltiples factores de riesgo, entre los que destaca el estado inflamatorio sistémico propio de pacientes obesos, que lleva a la progresión de la aterosclerosis. Profundizar en los mecanismos de esta relación resulta fundamental para el desarrollo de nuevas herramientas terapéuticas y profilácticas. Distintas investigaciones han demostrado la eficacia de la suplementación con ácidos grasos omega 3 en la disminución del estado inflamatorio, así como su acción sobre el metabolismo de los lípidos. Uno de los mecanismos que se han sugerido es que pueda actuar sobre la respuesta celular a la hipoxia que, en el tejido adiposo, podría ser la principal desencadenante de la inflamación y que determinará la evolución de los pacientes con cardiopatía isquémica o accidente cerebrovascular, que no suponen otra cosa que la interrupción del flujo sanguíneo a nivel coronario o cerebral. En este contexto, la presente revisión pretende determinar el estado de la investigación sobre el empleo de ácidos grasos omega 3 en el tratamiento y prevención de las principales enfermedades cardiovasculares por sus acciones frente a la hipoxia. A pesar de la heterogeneidad de los artículos revisados parece claro el efecto beneficioso de los ácidos grasos omega 3, aunque pocos parecen relacionarlo con su acción frente a la hipoxia. En estos últimos parece que el efecto estaría mediado por la angiogénesis y la actividad de VEGF y quizá podría estar implicada la regulación de HIF-1α. Si bien, parece clara la necesidad de una mayor investigación en este campo para detallar los mecanismos por los que actúan los omega 3 y la relación que podrían tener con la hipoxia.Ischemic heart disease and stroke are the leading causes of death worldwide. The development of both is conditioned by multiple risk factors, among which, the systemic inflammatory state characteristic of obese patients stands out, which leads to the progression of atherosclerosis. Studying the mechanisms of this relationship in depth is essential for the development of new therapeutic and prophylactic tools. Various investigations have shown the efficacy of omega 3 fatty acid supplementation in reducing the inflammatory state, as well as its action on lipid metabolism. One of the mechanisms that have been suggested is that it can act on the cellular response to hypoxia that, in adipose tissue, could be the main trigger for inflammation and that will determine the evolution of patients with ischemic heart disease or stroke, which only consist on the interruption of blood flow at coronary or cerebral level. In this context, this review aims to determine the state of the research on the use of omega 3 fatty acids in the treatment and prevention of the main cardiovascular diseases due to their actions against hypoxia. Despite the heterogeneity of the articles reviewed, the beneficial effect of omega 3 fatty acids seems clear, although few seem to relate these to their action against hypoxia. In the latter, it appears that the effect would be mediated by angiogenesis and VEGF activity, and perhaps, HIF-1α regulation might be involved. In any case, it seems clear the need for further research in this field to detail the mechanisms by which omega 3 act, and the relationship that they could have with hypoxia

The facilitated glucose transporter GLUT12: What do we know and what would we like to know?

Human GLUT12 was isolated from the breast cancer cell line MCF-7 by its homology with GLUT4. Glucose has been described as its main substrate, but it also can transport other sugars. In humans, GLUT12 protein is expressed mainly in insulin sensitive tissues. Functional analysis has showed that GLUT12 transports sugars down its concentration gradient, but it can also work as a proton-coupled symporter. Studies from our laboratory, performed in Xenopus laevis oocytes expressing GLUT12, show that glucose uptake increases in the presence of Na+ and induces inward current. These findings suggest a transport mechanism never described for other GLUTs, which would indicate a distinct functional role for GLUT12. In relation with its physiological and pathophysiological function, GLUT12 has been mainly studied due to its role as a secondary insulin-sensitive glucose transporter and its possible implication in impaired insulin signalling pathologies. Its expression in some tumour tissues has been described and recently, it has been proposed as one of the key proteins in the glucose supply to malignant cells. Overall, even though a lot of information about GLUT12 has been released during the last years, its functional characteristics, physiological role or implication in the development of some diseases is still unclear. Therefore, this review of the literature can help to address further investigations needed to elucidate these issues that, in our view, are of great interest mainly due to the direct GLUT12 relation with cancer and probably with diabetes development

Upregulation of the expression of inflammatory and angiogenic markers in human adipocytes by a synthetic cannabinoid, JTE-907

Inflammation in adipose tissue is a characteristic of obesity and the metabolic syndrome. It is suggested that the endocannabinoid system is involved in the regulation of infl ammatory and angiogenic processes within the tissue. Human subcutaneous preadipocytes (Zen Bio) were used as the source of human preadipocytes or adipocytes. Gene expression was examined by RT-PCR and real-time PCR. The secretion of infl ammation-related proteins was determined by an ELISA array. In experiments on adipocytes treated at day 14 post-diff erentiation, JTE-907, a synthetic cannabinoid, upregulated the expression of key infl ammatory markers – IL-6, MCP-1 and IL-1 β – and angiogenic factors – VEGF and ANGPTL4 – at 10 μ M after 20 h of treatment, having also increased the expression of TRPV1 at 10 μ M. JTE-907 showed no eff ect after 4 h. The ELISA array showed a 2.6-fold increase in IL-6 protein release. The eff ect of JTE-907 was inhibited by AM251 (CB 1 antagonist), and partially by arachidonyl serotonin (TRPV1 and FAAH antagonist). The CB 2 antagonist, AM630, partially upregulated the eff ect of JTE-907. Preadipocytes fed 14 days after 100 % confl uence exhibited downregulation of CB 1 , MCP-1, and IL-1 β , 20 h after having been exposed to JTE-907. CB 1 and TRPV1 receptors participate in the regulation of several infl ammatory and angiogenic factors in human adipocytes, indicating their potential value as targets for the treatment of disorders related to obesity

Influence of different oxygen supply on metabolic markers and gene response in murine adipocytes

Obese subjects often present a low-grade chronic inflammation in the white adipose tissue, which seems to play an important role in the initiation and development of obesity-related diseases. It has been reported that this inflammatory process may be due to a hypoxic state occuring whithin this tissue. Oxygen is used in current medicine as a treatment for several conditions. The aim of this study was to analyze the effects of 95% O2 on specific metabolic variables and on the expression of some adipokines on murine adipocytes. 3T3-L1 adipocytes were exposed during 48 h to different treatments: 95% O2 hyperoxia (HPx group), CoCl2 (CoCl2 group), hyperoxia with CoCl2 (HPx+CoCl2 group) and 1%O2 hypoxia (Hx group). Cell viability, intracellular ROS content, glucose utilization, lactate and glycerol concentrations were measured. Also, mRNA expression of HIF-1[alfa], GLUT-1, ANGPTL4, PPAR-[gamma], adiponectin, IL-6 and MCP-1 genes was analyzed. Importantly, 95% O2 decreased cell viability and increased intracellular ROS production. Also, glycerol and lactate release were significantly increased and decreased, respectively, in HPx treated cells. This treatment also provoked a downregulation of GLUT-1 and ANGPTL-4, while IL-6 and MCP-1 were up-regulated. Exposure to a hyperoxia of 95% O2 seemed to provoke an inflammatory response in adipocytes. The two hypoxia-inducing conditions (CoCl2 and 1% O2) produced different outcomes in metabolic measurements as well as in the expression of some genes (GLUT-1, ANPGTL4, PPAR-[gamma] and adiponectin), while it remained similar in others (HIF-1[alfa], IL-6 and MCP-1). Indeed, hyperoxia increased significantly the ROS levels and the lipolytic activity, while it reduced lactate production. In addition to the effects on inflammation, the changes in GLUT-1, ANGPTL4 and PPAR-[gamma] genes let suppose that hyperoxia may be beneficial for the hypertrophied adipose tissues of obese subjects and for improving insulin sensitivity

A dysregulation in CES1, APOE and other lipid metabolism-related genes is associated to cardiovascular risk factors linked to obesity

OBJECTIVE: The aim of the present study was to investigate the relationship between the differential expression of genes related to lipid metabolism in subcutaneous adipose tissue and metabolic syndrome features in lean and obese subjects with habitual high fat intake. METHODS: Microarray and RT-PCR analysis were used to analyze and validate differential gene expression in subcutaneous abdominal adipose tissue samples from lean and obese phenotype subjects. RESULTS: Several genes and transcripts involved in lipolysis were down-regulated, such as AKAP1, PRKAR2B, Gi and CIDEA, whereas NPY1R and CES1 were up-regulated, when comparing obese to lean subjects. Similarly, transcripts associated with cholesterol and lipoprotein metabolism showed a differential expression, with APOE and ABCA being decreased and VLDLR being increased in obese versus lean subjects. In addition, positive correlations were found between different markers of the metabolic syndrome and CES1 and NPY1R mRNA expressions, while APOE showed an inverse association with some of them. CONCLUSION: Different expression patterns in transcripts encoding for proteins involved in lipolysis and lipoprotein metabolism were found between lean and obese subjects. Moreover, the dysregulation of genes such as CES1 and APOE seems to be associated with some physiopathological markers of insulin resistance and cardiovascular risk factors in obesity

Intervención dietético-nutricional en la prevención de la deficiencia de hierro

En este artículo se expone evidencia científica sobre la anemia ferropénica fundamentalmente desde aspectos dietético-nutricionales que inciden en la biodisponibilidad del hierro de los alimentos. La anemia constituye un problema de salud pública a nivel mundial, padeciéndolo aproximadamente 2000 millones de personas y afectando fundamentalmente a lactantes, ancianos, adolescentes, mujeres en edad fértil y embarazadas. Como consecuencia de esta enfermedad, la capacidad para realizar trabajo físico, la inmunidad celular y la capacidad bactericida de los neutrófilos se ven sensiblemente alteradas. Además, la anemia puede producir: mayor susceptibilidad a infecciones, especialmente, del tracto respiratorio, disminución de la termogénesis en ambientes fríos, alteraciones funcionales del tubo digestivo, fallo en la movilización de la vitamina A hepática, disminución de la velocidad de crecimiento, alteraciones en el desarrollo mental y motor, menor transferencia de hierro al feto, mayor riesgo de parto prematuro o morbilidad perinatal, entre otras. Dentro de los factores que interfieren en la absorción del hierro, los dietéticos son de gran relevancia. Las proteínas cárnicas, ácidos orgánicos, la vitamina C y la A y los fructooligosacáridos (FOS), favorecen su absorción mientras que ciertas proteínas del huevo y de la leche, polifenoles, fitatos, fibra insoluble y minerales como el fósforo, calcio o el zinc, afectan negativamente a la biodisponibilidad del hierro. Las diferentes técnicas culinarias también pueden aumentar o disminuir la biodisponibilidad del hierro. La información recopilada sobre los factores favorecedores e inhibidores de la absorción del hierro, se ha utilizado para, a modo de conclusión, marcar unas pautas dietético-nutricionales para las personas que padecen o tienen predisposición a padecer anemia.This paper outlines the scientific evidence of iron deficiency anemia from dietary and nutritional issues that affect iron-bioavailability from food. Anemia is a worldwide public health problem, with about 2000 million people who suffer from it and mainly affects older infants, adolescents, women of childbearing age and pregnant women. As a consequence of this disease, alterations have been reported: in physical work capacity, cellular immunity and bactericidal capacity of neutrophils. Further more, an increased susceptibility to infections, specially respiratory tract, decreased thermogenesis in cold environments , functional disorders of the gastrointestinal tract, failure in the mobilization of liver vitamin A, decreased growth rate, impaired mental and motor development, less transfer of iron to the fetus, increased risk of preterm delivery, perinatal morbidity, and others. Among the factors that interfere with iron absorption, the diet is one of the most important. Meat proteins, organic acids, vitamin C and A and fructooligosaccharides (FOS), promote the absorption. While egg, milk proteins, polyphenols, phytates, fiber and minerals such as phosphorus, calcium or zinc affect negatively the ironbioavailability. The information collected about the stimulating factors and inhibitors of iron absorption has been used to, as a conclusion, make dietary and nutritional guidelines for those who are predisposed to suffer from anemia

Cerium oxide nanoparticles regulate insulin sensitivity and oxidative markers in 3T3-L1 adipocytes and C2C12 myotubes

Insulin resistance is associated with oxidative stress, mitochondrial dysfunction, and a chronic low-grade inflammatory status. In this sense, cerium oxide nanoparticles (CeO2 NPs) are promising nanomaterials with antioxidant and anti-inflammatory properties. Thus, we aimed to evaluate the effect of CeO2 NPs in mouse 3T3-L1 adipocytes, RAW 264.7 macrophages, and C2C12 myotubes under control or proinflammatory conditions. Macrophages were treated with LPS, and both adipocytes and myotubes with conditioned medium (25% LPS-activated macrophages medium) to promote inflammation. CeO2 NPs showed a mean size of ≤25.3 nm (96.7%) and a zeta potential of mV, suitable for cell internalization. CeO2 NPs reduced extracellular reactive oxygen species (ROS) in adipocytes with inflammation while increased in myotubes with control medium. The CeO2 NPs increased mitochondrial content was observed in adipocytes under proinflammatory conditions. Furthermore, the expression of Adipoq and Il10 increased in adipocytes treated with CeO2 NPs. In myotubes, both Il1b and Adipoq were downregulated while Irs1 was upregulated. Overall, our results suggest that CeO2 NPs could potentially have an insulin-sensitizing effect specifically on adipose tissue and skeletal muscle. However, further research is needed to confirm these findings

The association of parental genetic, lifestyle, and social determinants of health with offspring overweight

In the UK, the number of comorbidities seen in children has increased along with the worsening obesity rate. These comorbidities worsen into adulthood. Genomewide association studies have highlighted single nucleotide polymorphisms associated with the weight status of adults and offspring individually. To date, in the UK, parental genetic, lifestyle, and social determinants of health have not been investigated alongside one another as influencers of offspring weight status. A comprehensive obesity prevention scheme would commence prior to conception and involve parental intervention including all known risk factors. This current study aims to identify the proportion of overweight that can be explained by known parental risk factors, including genetic, lifestyle, and social determinants of health with offspring weight status in the UK. Methods: A crosssectional study was carried out on 123 parents. Parental and offspring anthropometric data and parental lifestyle and social determinants of health data were self-reported. Parental genetic data were collected by use of GeneFiX saliva collection vials and genotype were assessed for brain-derived neurotrophic factor (BDNF) gene rs6265, melanocortin 4 receptor (MC4R) gene rs17782313, transmembrane protein 18 (TMEM18) gene rs2867125, and serine/threonine-protein kinase (TNN13K) gene rs1514175. Associations were assessed between parental data and the weight status of offspring. Results: Maternal body mass index modestly predicted child weight status (p < 0.015; R2 = 0.15). More mothers of overweight children carried the MC4R rs17782313 risk allele (77.8%; p = 0.007) compared to mothers of normal-weight children. Additionally, fathers who were not Caucasian and parents who slept for < 7 h/night had a larger percentage of overweight children when compared to their counterparts (p = 0.039; p = 0.014, respectively). Conclusion: Associations exist between the weight status of offspring based solely on parental genetic, lifestyle, and social determinants of health data. Further research is required to appropriately address future interventions based on genetic and lifestyle risk groups on a pre-parent cohort

Usefulness of combining intermittent hypoxia and physical exercise in the treatment of obesity

Obesity is an important public health problem worldwide and is a major risk factor for a number of chronic diseases such as type 2 diabetes, adverse cardiovascular events and metabolic syndrome related features. Different treatments have been applied to tackle body fat accumulation and its associated clinical manifestations. Often, relevant weight loss is achieved during the first six months under different dietary treatments. From this point, a plateau is reached, and a gradual recovery of the lost weight may occur. Therefore, new research approaches are being investigated to assure weight maintenance. Pioneering investigations have reported that oxygen variations in organic systems may produce changes in body composition. Possible applications of intermittent hypoxia to promote health and in various pathophysiological states have been reported. The hypoxic stimulus in addition to diet and exercise can be an interesting approach to lose weight, by inducing higher basal noradrenalin levels and other metabolic changes whose mechanisms are still unclear. Indeed, hypoxic situations increase the diameter of arterioles, produce peripheral vasodilatation and decrease arterial blood pressure. Furthermore, hypoxic training increases the activity of glycolytic enzymes, enhancing the number of mitochondria and glucose transporter GLUT-4 levels as well as improving insulin sensitivity. Moreover, hypoxia increases blood serotonin, decreases leptin levels while appetite is suppressed. These observations allow considering the hypothesis that intermittent hypoxia induces fat loss and may ameliorate cardiovascular health, which might be of interest for the treatment of obesity. This new strategy may be useful and practical for clinical applications in obese patients