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When looking for new ingredients to process red meat, poultry, and fish products, it is essential to consider using vegetable resources that can replace traditional ingredients such as animal fat and synthetic antioxidants that may harm health. The Amazon, home to hundreds of edible fruit species, can be a viable alternative for new ingredients in processing muscle food products. These fruits have gained interest for their use as natural antioxidants, fat replacers, colorants, and extenders. Some of the fruits that have been tested include açai, guarana, annatto, cocoa bean shell, sacha inchi oil, and peach palm. Studies have shown that these fruits can be used as dehydrated products or as liquid or powder extracts in doses between 250 and 500 mg/kg as antioxidants. Fat replacers can be added directly as flour or used to prepare emulsion gels, reducing up to 50% of animal fat without any detrimental effects. However, oxidation problems of the gels suggest that further investigation is needed by incorporating adequate antioxidant levels. In low doses, Amazon fruit byproducts such as colorants and extenders have been shown to have positive technological and sensory effects on muscle food products. While evidence suggests that these fruits have beneficial health effects, their in vitro and in vivo nutritional effects should be evaluated in muscle food products containing these fruits. This evaluation needs to be intended to identify safe doses, delay the formation of key oxidation compounds that directly affect health, and investigate other factors related to health.
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Heart failure (HF) is a heterogeneous condition that can be categorized according to the left ventricular ejection fraction (EF) into HF with reduced (HFrEF) or preserved (HFpEF) EF. Although HFrEF and HFpEF share some common clinical manifestations, the mechanisms underlying each phenotype are often found to be distinct. Identifying shared and divergent pathophysiological features might expand our insights on HF pathophysiology and assist the search for therapies for each HF subtype. In this study, we evaluated and contrasted two new murine models of non-ischaemic HFrEF and cardiometabolic HFpEF in terms of myocardial structure, left ventricular function, gene expression, cardiomyocyte calcium handling, mitochondrial polarization and protein acetylation in a head-to-head fashion. We found that in conditions of similar haemodynamic stress, the HFrEF myocardium underwent a more pronounced hypertrophic and fibrotic remodelling, whereas inflammation was greater in the HFpEF myocardium. We observed opposing features on calcium release, which was diminished in the HFrEF cardiomyocyte but enhanced in the HFpEF cardiomyocyte. Mitochondria were less polarized in both HFrEF and HFpEF cardiomyocytes, reflecting similarly impaired metabolic capacity. Hyperacetylation of cardiac proteins was observed in both models, but it was more accentuated in the HFpEF heart. Despite shared features, unique triggering mechanisms (neurohormonal overactivation in HFrEF vs. inflammation in HFpEF) appear to determine the distinct phenotypes of HF. The findings of the present research stress the need for further exploration of the differential mechanisms underlying each HF subtype, because they might require specific therapeutic interventions. KEY POINTS: The mechanisms underlying heart failure with either reduced (HFrEF) or preserved (HFpEF) ejection fraction are often found to be different. Previous studies comparing pathophysiological traits between HFrEF and HFpEF have been conducted on animals of different ages and strains. The present research contrasted two age-matched mouse models of non-ischaemic HFrEF and cardiometabolic HFpEF to uncover divergent and shared features. We found that upon similar haemodynamic stress, the HFrEF heart experienced a more pronounced hypertrophic and fibrotic remodelling, whereas inflammation appeared to be greater in the HFpEF myocardium. Calcium release was diminished in the HFrEF cardiomyocyte and enhanced in the HFpEF cardiomyocyte. Mitochondria were comparably less polarized in both HFrEF and HFpEF myocytes. Hyperacetylation of proteins was common to both models, but stronger in the HFpEF heart. Casting light on common and distinguishing features might ease the quest for phenotype-specific therapies for heart failure patients.
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Meat products are known for their lipid profile rich in saturated fats and cholesterol, and also for the formation of oxidation compounds; therefore, a reduction in animal fat may result in a product less harmful to health. Pijuayo is an Amazon fruit known for its nutritional properties, such as its fiber and lipid content. For these reasons, it is an attractive fruit to replace animal fat in meat products. The present work used pijuayo pulp and peel flours to partially replace animal fat in beef-based burgers at 25% and 50% levels, considering sensory and physicochemical outcomes evaluated by Principal Component Analysis (PCA), Correspondence Analysis (CA) and Multiple Factor Analysis (MFA). Pijuayo flour affected the physicochemical characteristics evaluated by PCA, where the samples with greater fat replacement were characterized by a high carbohydrate content and instrumental yellowness. The minimal fat replacement did not abruptly affect the PCA's instrumental texture and color, proximal composition, yield properties, and lipid oxidation. The overall liking was greater in the 25% fat reduction treatments, even greater than the control, in which positive sensory attributes for liking were highlighted for those treatments. A small segment of consumers (11% of total consumers) preferred the treatment with greater replacement of fat with pijuayo peel flour, which these consumers tended to characterize as seasoned. However, this treatment had the lowest liking. The MFA showed that the sensory characteristics tender and tasty were strongly correlated with overall liking and were highlighted in the samples of 25% fat reduction, suggesting that the pijuayo improves the tenderness and flavor of reduced-fat burgers. Other inclusion levels between 25% and 50% of fat replacement could be explored, and optimization studies are needed. In addition, the sensory characteristics and flavor-enhancing compounds of the fruit, as well as the nutritional aspects of the inclusion of pijuayo, should be studied, such as the fatty acid profile. These characteristics will be informative to explore pijuayo as a fat replacer at a pilot scale and industrial scale.
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Maternal nutritional programming by energy-dense foods leads to the transgenerational heritance of addiction-like behavior. Exposure to energy-dense foods also activates systemic and central inflammation in the offspring. This study aimed to characterize pro- and anti-inflammatory cytokine profiles in blood and their correlation to the transgenerational heritance of the addiction-like behavior in rats. F1 offspring of male Wistar diagnosed with addiction-like behavior were mated with virgin females to generate the F2 and the F3 offspring, respectively. Diagnosis of addiction-like behavior was performed by the operant training schedule (FR1, FR5 and PR) and pro- and anti-inflammatory cytokine profiles in blood were measured by multiplex platform. Multiple linear models between behavior, fetal programming by diet and pro- and anti-inflammatory cytokine profiles were performed. We found that the addiction-like behavior found in the F1 male offspring exposed to energy-dense food (cafeteria, CAF) diet during fetal programing is transgenerational inherited to the F2 and F3 generations. Blood from addiction-like behavior subjects of F2 and F3 generations exposed to CAF diet during maternal programming showed decrease in the anti-inflammatory IL-10 in the plasma. Conversely, decreased levels of the pro-inflammatory MCP-1 was identified in non-addiction-like subjects. No changes were found in plasmatic TNF-α levels in the F2 and F3 offspring of non-addiction-like and addiction-like subjects. Finally, biological modeling between IL-10 or MCP-1 plasma levels and prenatal diet exposure on operant training responses confirmed an association of decreased IL-10 levels on addiction-like behavior in the F2 and F3 generations. Globally, we identified decreased anti-inflammatory IL-10 cytokine in the blood of F2 and F3 offspring subjects diagnosed with addiction-like behavior for food rewards.
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Adicción a la Comida , Efectos Tardíos de la Exposición Prenatal , Animales , Antiinflamatorios , Condicionamiento Operante , Femenino , Humanos , Interleucina-10 , Masculino , Embarazo , Ratas , Ratas WistarRESUMEN
Autism spectrum disorder (ASD) is a disease characterized by reduced social interaction and stereotypic behaviors and related to macroscopic volumetric changes in cerebellar and somatosensory cortices (SPP). Epidemiological and preclinical models have confirmed that a proinflammatory profile during fetal development increases ASD susceptibility after birth. Here, we aimed to globally identify the effect of maternal exposure to high-energy dense diets, which we refer to as cafeteria diet (CAF) on peripheral and central proinflammatory profiles, microglia reactivity, and volumetric brain changes related to assisting defective social interaction in the mice offspring. We found a sex-dependent effect of maternal exposure to CAF diet or inoculation of the dsARN mimetic Poly (I:C) on peripheral proinflammatory and social interaction in the offspring. Notably, maternal exposure to CAF diet impairs social interaction and favors an increase in anxiety in male but not female offspring. Also, CAF diet exposure or Poly (I:C) inoculation during fetal programming promote peripheral proinflammatory profile in the ASD-diagnosed male but not in females. Selectively, we found a robust accumulation of the monocyte chemoattractant protein-1 (MCP-1) in plasma of ASD-diagnosed males exposed to CAF during fetal development. Biological assessment of MCP-1 signaling in brain confirms that systemic injection of MCP-1-neutralizing antibody reestablished social interaction and blocked anxiety, accompanied by a reduction in cerebellar lobule X (CbX) volume and an increase volume of the primary somatosensory (SSP) cortex in male offspring. These data highlight the contribution of diet-dependent MCP-1 signaling on volumetric brain changes and microglia morphology promoting ASD-like behavior in male mice.
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Trastorno del Espectro Autista , Quimiocina CCL2 , Efectos Tardíos de la Exposición Prenatal , Animales , Trastorno del Espectro Autista/metabolismo , Trastorno del Espectro Autista/patología , Encéfalo/anatomía & histología , Encéfalo/metabolismo , Quimiocina CCL2/metabolismo , Femenino , Masculino , Ratones , Microglía/citología , Embarazo , Conducta SocialRESUMEN
Fetal programming by hypercaloric intake leads to food addiction-like behavior and brain pro-inflammatory gene expression in offspring. The role of methylome modulation during programming on central immune activation and addiction-like behavior has not been characterized. We employed a nutritional programming model exposing female Wistar rats to chow diet, cafeteria (CAF), or CAF-methyl donor's diet from pre-pregnancy to weaning. Addiction-like behavior in offspring was characterized by the operant training response using Skinner boxes. Food intake in offspring was determined after fasting-refeeding schedule and subcutaneous injection of ghrelin. Genome-wide DNA methylation in the nucleus accumbens (NAc) shell was performed by fluorescence polarization, and brain immune activation was evaluated using real-time PCR for pro-inflammatory cytokines (IL-1ß, TNF-1α, and IL-6). Molecular effects of methyl modulators [S-adenosylmethionine (SAM) or 5-azatidine (5-AZA)] on pro-inflammatory cytokine expression and phagocytosis were identified in the cultures of immortalized SIM-A9 microglia cells following palmitic acid (100 µM) or LPS (100 nM) stimulation for 6 or 24 h. Our results show that fetal programming by CAF exposure increases the number of offspring subjects and reinforcers under the operant training response schedule, which correlates with an increase in the NAc shell global methylation. Notably, methyl donor's diet selectively decreases lever-pressing responses for reinforcers and unexpectedly decreases the NAc shell global methylation. Also, programmed offspring by CAF diet shows a selective IL-6 gene expression in the NAc shell, which is reverted to control values by methyl diet exposure. In vitro analysis identified that LPS and palmitic acid activate IL-1ß, TNF-1α, and IL-6 gene expression, which is repressed by the methyl donor SAM. Finally, methylation actively represses phagocytosis activity of SIM-A9 microglia cells induced by LPS and palmitic acid stimulation. Our in vivo and in vitro data suggest that fetal programming by methyl donors actively decreases addiction-like behavior to palatable food in the offspring, which correlates with a decrease in NAc shell methylome, expression of pro-inflammatory cytokine genes, and activity of phagocytic microglia. These results support the role of fetal programming in brain methylome on immune activation and food addiction-like behavior in the offspring.
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Maternal overnutrition modulates body weight, development of metabolic failure and, potentially, neurodegenerative susceptibility in the offspring. Overnutrition sets a chronic pro-inflammatory profile that integrates peripheral and central immune activation nodes, damaging neuronal physiology and survival. Innate immune cells exposed to hypercaloric diets might experience trained immunity. Here, we address the role of maternal overnutrition as a trigger for central and peripheral immune training and its contribution to neurodegeneration and the molecular nodes implicated in the Nod-like receptor protein 3 (NLRP3) inflammasome pathway leading to immune training. We propose that maternal overnutrition leads to peripheral or central immune training that favor neurodegenerative susceptibility in the offspring.
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Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have not been fully clarified. Maternal immune activation (MIA) during pregnancy have been proposed as a potential etiological cause leading to aberrant synaptic pruning and microglia-mediated neurogenesis impairment. Several clinical studies suggest that pro-inflammatory profile during maternal obesity associates with a higher risk of having a child with autism. In this context, the effect of maternal programing by high fat diet overconsumption during pregnancy sets a pro-inflammatory profile partly dependent on an epigenetic program of immunity which promotes brain micro and macrostructural abnormalities in the offspring that might last through adulthood accompanied by phenotypic changes in ASD subjects. Of note, maternal programming of inflammation during development seems to integrate the CNS and peripheral immune system cross-talk which arrays central inflammatory domains coordinating ASD behavior. In this review, we discuss basic and clinical studies regarding the effects of obesity-induced MIA on peripheral immune cells and microglia priming and their relationship with brain structural alterations in ASD models. Also, we show supportive evidence stating the role of maternal programming on epigenetic gene activation in immune cells of ASD subjects. We suggest that maternal programming by hypercaloric diets during development sets a central and peripheral immune cross-talk which potentially might modulate brain macro and microstructural defects leading to autism susceptibility.
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Trastorno del Espectro Autista/metabolismo , Dieta Alta en Grasa/efectos adversos , Susceptibilidad a Enfermedades/metabolismo , Mediadores de Inflamación/metabolismo , Hipernutrición/metabolismo , Efectos Tardíos de la Exposición Prenatal/metabolismo , Animales , Trastorno del Espectro Autista/inducido químicamente , Trastorno del Espectro Autista/inmunología , Susceptibilidad a Enfermedades/inducido químicamente , Susceptibilidad a Enfermedades/inmunología , Epigénesis Genética/fisiología , Femenino , Humanos , Mediadores de Inflamación/inmunología , Salud Materna , Obesidad/complicaciones , Obesidad/inmunología , Obesidad/metabolismo , Hipernutrición/complicaciones , Hipernutrición/inmunología , Embarazo , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Efectos Tardíos de la Exposición Prenatal/inmunologíaRESUMEN
Obesity or maternal overnutrition during pregnancy and lactation might have long-term consequences in offspring health. Fetal programming is characterized by adaptive responses to specific environmental conditions during early life stages. Programming alters gene expression through epigenetic modifications leading to a transgenerational effect of behavioral phenotypes in the offspring. Maternal intake of hypercaloric diets during fetal development programs aberrant behaviors resembling addiction in offspring. Programming by hypercaloric surplus sets a gene expression pattern modulating axonal pruning, synaptic signaling, and synaptic plasticity in selective regions of the reward system. Likewise, fetal programming can promote an inflammatory phenotype in peripheral and central sites through different cell types such as microglia and T and B cells, which contribute to disrupted energy sensing and behavioral pathways. The molecular mechanism that regulates the central and peripheral immune cross-talk during fetal programming and its relevance on offspring's addictive behavior susceptibility is still unclear. Here, we review the most relevant scientific reports about the impact of hypercaloric nutritional fetal programming on central and peripheral inflammation and its effects on addictive behavior of the offspring.
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Conducta Adictiva , Fenómenos Fisiologicos Nutricionales Maternos , Hipernutrición , Efectos Tardíos de la Exposición Prenatal , Animales , Femenino , Desarrollo Fetal , Inflamación , Obesidad , EmbarazoRESUMEN
Central nervous system (CNS) senses energy homeostasis by integrating both peripheral and autonomic signals and responding to them by neurotransmitters and neuropeptides release. Although it is previously considered an immunologically privileged organ, we now know that this is not so. Cells belonging to the immune system, such as B and T lymphocytes, can be recruited into the CNS to face damage or infection, in addition to possessing resident immunological cells, called microglia. In this way, positive energy balance during obesity promotes an inflammatory state in the CNS. Saturated fatty acids from the diet have been pointed out as powerful candidates to trigger immune response in peripheral system and in the CNS. However, how central immunity communicates to peripheral immune response remains to be clarified. Recently there has been a great interest in the neuropeptides, POMC derived peptides, ghrelin, and leptin, due to their capacity to suppress or induce inflammatory responses in the brain, respectively. These may be potential candidates to treat different pathologies associated with autoimmunity and inflammation. In this review, we will discuss the role of lipotoxicity associated with positive energy balance during obesity in proinflammatory response in microglia, B and T lymphocytes, and its modulation by neuropeptides.
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Sistema Nervioso Central/metabolismo , Inflamación/metabolismo , Neuropéptidos/metabolismo , Obesidad/metabolismo , Animales , Autoinmunidad/fisiología , Linfocitos B/metabolismo , Humanos , Microglía/metabolismo , Linfocitos T/metabolismoRESUMEN
En este proyecto se plantea un problema de repercusión en la salud pública: el diagnóstico tardío de la DEC. El objetivo general del estudio es determinar los casos de DEC diagnosticados tardadamente en el periodo establecido, que fueron internados en el HNN, con el fin de concientizar a la comunidad médica sobre la magnitud del problema, sus complicaciones potenciales irreversibles y enfatizar la importancia de la detección temprana. Métodos: Este es un estudio retrospectivo que analiza expedientes médicos de pacientes internados con el diagnóstico de DEC en el HNN, de 1996 a 2000. La muestra fue escogida de manera aleatoria. Los datos se organizaron en un instrumento de recolección y se analizaron de acuerdo con las tasas, promedio, porcentajes y relaciones entre ellos. Resultados: La mayor incidencia de casos de DEC se da en San José, seguida por Cartago y en tercer lugar, Heredia. La mayoría de los pacientes fueron diagnosticados en el periodo comprendido entre el primero y los cinco años. La edad promedio de la muestra fue de 3 años y 4 meses, con una desviación estándar de 4.99. Se encontró que el 82 por ciento de los pacientes fueron del sexo femenino y el 18 por ciento del masculino. El tipo de luxación más frecuente fue la izquierda, en un 55.2 por ciento casos; la luxación derecha correspondió a un 24.8 por ciento, y la bilateral a un 20.0 por ciento. La relación entre izquierda y derecha fue de 2.2:1. Al nacer, presentación fetal más frecuente fue la cefálica, en un 62.9 por ciento de los pacientes. La presentación pélvica representó, un 26.7 por ciento y en un 10.5 por ciento de los afectados, no se indicó. En cuanto al tipo de parto, un 80 por ciento fue vaginal y un 19 por ciento por cesárea, en un 7 por ciento, no se indica. El porcentaje de niños nacidos de término fue de un 67.6 por ciento. Conclusiones: Dentro de la población de estudio, la mayor parte de los pacientes fueron diagnosticados después del año, cuando el defecto se hizo evidente por el inicio de la bipedestación. De toda la población de estudio, el 98,5 por ciento fue sometida a algún tipo de tratamiento quirúrgico. La intervención quirúrgica, además de representar un alto costo institucional, constituye un trauma para el paciente, los resutados no siempre son óptimos y las complicaciones son diversas. Palabras clave: Displasia evolutiva cadera, diagnóstico.