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1.
J. physiol. biochem ; 72(1): 25-32, mar. 2016. tab, graf
Artigo em Inglês | IBECS | ID: ibc-168204

RESUMO

Obesity, a complex metabolic disorder, is characterized by mitochondrial dysfunction and oxidative stress. Increased expression of uncoupling protein 2 (UCP2) during obesity is an adaptive response to suppress the production of reactive oxygen species. The aims of this study were to compare the expression of UCP2 in diet-induced obese Wistar rats that differed according to age and their severity of obesity, and to compare UCP2 expression in the liver and muscle of these rats. UCP2 messenger RNA and protein expression was increased 4.6-fold (p < 0.0001) and 3.0-fold (p < 0.05), respectively, in the liver of the older and heavier rats. In contrast, UCP2 expression was decreased twofold (p < 0.005) in the muscle of these rats, while UCP3 messenger RNA (mRNA) was increased twofold (p < 0.01). Peroxisome proliferator-activated receptor alpha (PPARα) was similarly increased (3.0-fold, p < 0.05) in the liver of the older and more severe obese rats. Total protein content was increased (2.3-fold, p < 0.0001), while 5' adenosine monophosphate-activated protein kinase (AMPK) activity was decreased (1.3-fold, p = 0.05) in the liver of the older, heavier rats. No difference in total protein content and AMPK expression was observed in the muscle of these rats. This study showed that the expression of UCP2 varies according to age and the severity of obesity and supports the widely held notion that increased UCP2 expression is an adaptive response to increased fatty acid β-oxidation and reactive oxygen species production that occurs during obesity. An understanding of metabolic adaptation is imperative to gain insight into the underlying causes of disease, thus facilitating intervention strategies to combat disease progression (AU)


No disponible


Assuntos
Animais , Masculino , Ratos , Obesidade/metabolismo , Fatores Etários , Proteínas Mitocondriais/metabolismo , Canais Iônicos/metabolismo , Ratos Wistar , Proteína Desacopladora 2
2.
Arch. med. deporte ; 32(165): 25-31, ene.-feb. 2015. graf
Artigo em Inglês | IBECS | ID: ibc-139220

RESUMO

Physical training in animal models promotes changes that can be extrapolated to humans, due to physiological similarities between these species. Thus, the use of rodents submitted to exercise becomes feasible due to the possibility of analyzing variables that would not be admissible in humans. The aim of this study was to evaluate the effects of six weeks of swimming, at moderate intensity, on physical and physiological parameters of Wistar rats. Twelve animals were divided into two groups (trained and non-trained). The trained animals were subjected to six weeks of aerobic training in water with 5% of body weight load. The results between groups were compared by the t test (p < 0.05). The variation in body weight was lower in the trained groups. Food and water consumption were higher in the animals submitted to physical training. The relative weight of heart and kidney were higher in trained animals, with no differences in the liver and gastrocnemius relative weight. The gastrocnemius muscle fiber diameter did not differ between groups. The training promoted an increase in the percentage of protein in the carcass and a decrease in body fat percentage, as well as in the diameter of the epididymal region adipocytes. Additionally, the training promoted increased levels of High Density Lipoproteins (HDL-C) and decreased levels of Low Density Lipoproteins (LDL-C) and triacylglycerols (TAG). It was concluded that six weeks of moderate-intensity aerobic training is sufficient to promote improvements in the metabolic profile, weight control, and reduce body fat and increase the protein content in the carcass of rats


El entrenamiento físico en un modelo animal promueve cambios que se pueden extrapolar a los seres humanos, debido a las similitudes fisiológicas entre estas especies. El uso de roedores sujetos a ejercicio se vuelve factible debido a la posibilidad de analizar variables que no serían aceptables en los seres humanos. El objetivo de este estudio fue evaluar los efectos de seis semanas de natación a una intensidad moderada en parámetros corporales y fisiológicos de ratas Wistar. Fueron divididos doce animales en dos grupos (entrenados y no entrenados). Las ratas entrenadas fueron sometidas a seis semanas de entrenamiento aeróbico en un medio acuático con una carga relativa a un 5% de su peso corporal. Los resultados entre los grupos se compararon por t-test de student (p < 0,05). La variación de la ganancia de peso corporal fue menor en los animales entrenados. El consumo de agua y alimentos fue mayor en los animales del grupo sometidos a entrenamiento. El peso relativo del corazón y de los riñones fue mayor en los animales entrenados, sin diferencias en el peso relativo del hígado gastrocnemio. El diámetro de las fibras del musculo no difirió entre los grupos. El entrenamiento provoco un aumento en el porcentaje de proteína en la carcasa y una disminución en el porcentaje de grasa corporal, así como en el diámetro de los adipocitos de la región del epidídimo. Además, el entrenamiento provoco un aumento de los niveles de lipoproteínas de alta densidad (HDL-C) y una disminución de los niveles de lipoproteína de baja densidad (LDL-C) y triacilgliceridos (TAG). Se concluye que seis semanas de entrenamiento aeróbico a una intensidad moderada es suficiente para promover mejoras en el perfil metabólico, control de peso, reducir la grasa corporal y aumentar el contenido de proteínas en la carcasa de las ratas


Assuntos
Animais , Ratos , Natação , Exercício Físico , Metabolismo/fisiologia , Composição Corporal , HDL-Colesterol/metabolismo , LDL-Colesterol/metabolismo , VLDL-Colesterol/metabolismo , Triglicerídeos/metabolismo , Proteínas Mitocondriais/biossíntese , Metabolismo dos Lipídeos , Consumo de Alimentos , Ingestão de Líquidos , Perda de Peso , Peso Corporal , Impactos na Saúde/prevenção & controle , Modelos Animais , Metabolismo Energético , Ratos Wistar , Parâmetros , Doenças Cardiovasculares/prevenção & controle
3.
Rev. esp. geriatr. gerontol. (Ed. impr.) ; 45(3): 156-166, abr.-jun. 2010. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-79808

RESUMO

Las proteínas mitocondriales pueden ser modificadas por reacciones de glicación inducidas por compuestos dicarbonilo procedentes del metabolismo tales como el glioxal y el metilglioxal. Estas modificaciones provocan cambios estructurales y funcionales en las proteínas implicadas. La modificación del proteoma mitocondrial por estos compuestos dicarbonilo puede inducir disfunción mitocondrial y acentuar un estado de estrés oxidativo. Así, estas modificaciones químicas podrían jugar un papel clave en el proceso fisiológico de envejecimiento y patologías asociadas a la edad, donde se han evidenciado tanto defectos de la actividad mitocondrial como incrementos de compuestos dicarbonilo. Identificar las proteínas mitocondriales especificamente modificadas, aseverar los cambios funcionales derivados y sus implicaciones constituyen lineas de investigación que tendrán su desarrollo en los próximos años(AU)


Mitochondrial proteins can be modified by glycation reactions from endogenous dicarbonyl compounds such as physiologically generated methylglyoxal and glyoxal. This modification could cause structural and functional changes in the proteins Consequently, dicarbonyl attack of the mitochondrial proteome may be an event leading to mitochondrial dysfunction and thus, to oxidative stress. These protein chemical modifications can play an important role in the physiological aging process and age-associated diseases, where both mitochondrial deffects and increased dicarbonyl concentrations have been found. Future research should address the functional changes in mitochondrial proteins that are the targets for dicarbonyl glycation(AU)


Assuntos
Humanos , Masculino , Feminino , Idoso , Proteínas Mitocondriais/metabolismo , Estresse Oxidativo/fisiologia , Produtos Finais de Glicação Avançada/metabolismo , Envelhecimento/fisiologia , Carbonilação Proteica/fisiologia , Proteoma
4.
Arch. Fac. Med. Zaragoza ; 49(2): 58-62, sept. 2009.
Artigo em Espanhol | IBECS | ID: ibc-114307

RESUMO

La deficiencia de la HMG-CoA sintasa mitocondrial (mHS) (MIM600234) es un error innato del metabolismo de tipo autosómico recesivo que está causada por mutaciones en el gen HMGCS2. La mHS es una enzima mitocondrial que cataliza el paso de condensación de acetil-CoA con acetoacetil-CoA para forma 3-hidroxi-2-metilgutaril CoA en la ruta de síntesis de los cuerpos cetónicos. Esta deficiencia suele aparecer en la primara infancia en situaciones de ayuno y alto consumo energético. Las manifestaciones clínicas son inespecíficas e incluyen vómitos, letargia y a veces coma. Hasta la fecha, sólo se han diagnosticado a nivel clínico y genético ocho pacientes en todo el mundo (AU)


The HMG-CoA synthase mitocondrial (mHS) deficiency (OMIM 600234) is an autosomal recessive inborn error of metabolism caused by mutations in the HMGCS2 gene. mHS is a mitochondrial enzyme that cathalyzes the condensation step of acetyl-CoA with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl CoA in the synthesis pathway of the ketone bodies. This deficiency frequently appears during childhood under fasting and/or high energy consumption situations. Clinical manifestations are rather inespecific and include vomiting, lethargy and, in some cases, coma. To date, only eight patients have been clinically and genetically characterized around the word (AU)


Assuntos
Humanos , Proteínas Mitocondriais/deficiência , Erros Inatos do Metabolismo/genética , Hidroximetilglutaril-CoA Sintase/deficiência , Fatores de Risco , Proteínas de Grupo de Alta Mobilidade/deficiência
5.
J. physiol. biochem ; 63(4): 317-328, oct.-dic. 2007. ilus, tab, graf
Artigo em Inglês | IBECS | ID: ibc-76686

RESUMO

The aim of the present work was to assess whether changes in adipose tissue geneexpression related with adipogenesis and/or thermogenesis could be involved in themechanism conferring susceptibility or resistance to develop obesity in high-fat fedoutbreed rats. For this purpose, male Wistar rats were fed with standard laboratorydiet (control group) or high fat diet. After 15 days, two groups of rats with significantdifferences on body weight gain in response to the high fat diet were characterizedand identified as diet-induced obesity (DIO) and diet resistant (DR) rats. A significantincrease in visceral white adipose tissue (WAT) PPARã and aP2 (p<0.05)mRNA levels associated to a decrease in RARã expression (p<0.05) was observed inDIO rats, suggesting an increase of adipogenesis. Furthermore, our data showed amarked increase in brown adipose tissue (BAT) of UCP1 mRNA in DIO animals(p<0.01) (without affecting PGC-1á gene expression), whereas no changes werefound in WAT UCP2 gene expression. All these data suggest that the variationsfound in the expression pattern of PPARã, aP2 and RARã by high-fat diet could beinvolved, at least in part, in the differences in body weight gain and adiposityobserved between DR and DIO animals. The compensatory adaptations through theincrease in energy expenditure by changes on the expression levels of UCP1 seem notto be enough to avoid the obesity onset in the DIO group (AU)


No disponible


Assuntos
Animais , Ratos , Adipogenia/genética , Tecido Adiposo/metabolismo , Gorduras na Dieta/administração & dosagem , Obesidade/genética , Termogênese/genética , Fatores de Transcrição/genética , Proteínas de Ligação a RNA/genética , Predisposição Genética para Doença/genética , Canais Iônicos/genética , Proteínas Mitocondriais/genética , Peso Corporal/genética
6.
Rev. Med. Univ. Navarra ; 51(3): 13-18, jul.-sept. 2007. ilus
Artigo em Espanhol | IBECS | ID: ibc-057581

RESUMO

La obesidad, una enfermedad con creciente prevalencia, se genera porun desequilibrio energético que podría relacionarse, en algunos casos,con la efi ciencia de la maquinaria energética celular en la que participanlas mitocondrias. Estos orgánulos son responsables del proceso defosforilación oxidativa, que concluye con la transformación de nutrientesen energía y ATP, generando radicales libres de alto poder oxidativo.Durante este proceso, estos agentes prooxidantes pueden ocasionardaño celular, que en cierta medida puede ser parcialmente neutralizadomediante factores antioxidantes endógenos como el glutatión, o deagentes antioxidantes aportados a través de la dieta.El descubrimiento de las proteínas desacoplantes mitocondriales (UCPs)abrió un nuevo campo de investigación. Así, la UCP1 o termogenina,encargada de la disipación de energía en forma de calor, disminuye lacantidad de ATP y ROS formadas y obligando a la célula que expresala UCP1 a oxidar más nutrientes para obtener energía. También se hanrealizado estudios genéticos sobre variantes de UCP2 y UCP3 que lasrelacionan con una cierta implicación en la obesidad


Obesity, an increasing prevalent disease, appears as a consequence of anenergetic umbalance that might be related to the effi ciency of the cellularenergetic machinery involving the mitochondria. In this organelle takesplace the oxidative phosphorylation, that ends with the transformationof the nutrients to energy and the ATP production. During this process,free radicals of high oxidative power maybe blocked by endogenousantioxidants like the glutathion, in collaboration with the contributionof antioxidants supplied by the diet.The discovery of mitochondrial uncoupling proteins (UCPs) opened anew fi eld of investigation, emphasizing the role of UCP1 or thermogenin,which generates an energy dissipation as heat and diminishing theamount of formed ATP and ROS and forcing the cell that expresses theUCP1 to oxidize more nutrients to obtain energy. Also, genetic studieshave been carried out about UCP2 and UCP3 polymorphisms that relatethem to obesity


Assuntos
Humanos , Obesidade/metabolismo , Mitocôndrias/metabolismo , Metabolismo Energético/fisiologia , Obesidade/etiologia , Proteínas Mitocondriais/metabolismo
7.
Nutr. hosp ; 21(1): 52-56, ene.-feb. 2006. tab
Artigo em Espanhol | IBECS | ID: ibc-045429

RESUMO

OBJETIVO: En el presente estudio se pretende evaluar la prevalencia de la mutación -866 G/A del gen de la UCP2 y conocer su influencia sobre el fenotipo de los niños (11- 12 años) navarros obesos. ANTECEDENTES Y ÁMBITO DEL ESTUDIO: La obesidad es una enfermedad de origen multifactorial, que puede estar relacionada con la presencia de mutaciones y polimorfismos en diversos genes candidatos. El gen de la proteína desacoplante UCP2 es uno de los más estudiados en relación con la obesidad porque parece participar en el control de la composición corporal y de diversos procesos metabólicos. Se han descrito tres polimorfismos en este gen: una inserción/deleción de 45 nucleótidos, un cambio del nucleótido guanina por adenina en la posición -866 y otro que origina un reemplazo de alanina por valina en el aminoácido 55. Según diferentes estudios, el alelo - 866G está relacionado con un mayor riesgo de desarrollar obesidad, aunque en la literatura aparecen resultados contradictorios en cuanto a esta asociación. SUJETOS: El estudio se llevó a cabo en 125 niños (52% varones) obesos de 11-12 años de edad, seleccionados a través de los Servicios de Endocrinología Pediátrica de la Clínica Universitaria y del Hospital Virgen del Camino (Pamplona), obteniendo el consentimiento informado de acuerdo con la declaración de Helsinki. INTERVENCIONES: Tras verificar el cumplimiento de los criterios de inclusión se tomaron medidas antropométricas (peso, talla, IMC, pliegue tricipital y subescapular) y se determinó el porcentaje de masa grasa por medio de impedancia bioeléctrica. Además se midieron los niveles plasmáticos de colesterol total, glucosa, insulina y leptina. Se procedió también a la extracción del ADN de las células sanguíneas de la serie blanca para determinar el genotipo mediante la técnica de PCR seguida de una digestión con BstUI y posterior visualización en un gel de agarosa con un 2% de bromuro de etidio. RESULTADOS: El análisis genético reveló una frecuencia del alelo A de 0,404, con un porcentaje de individuos G/G, G/A, y A/A del 40,0%, 39,2% y 20,8%, respectivamente. Los portadores del alelo A presentaron un valor significativamente mayor de la suma de los pliegues tricipital y subescapular (p=0,034). No se observaron diferencias significativas entre los sujetos mutados y los no mutados en cuanto a las variables bioquímicas estudiadas. CONCLUSIONES: Los sujetos portadores del polimorfismo presentan valores más altos para los pliegues tricipital y subescapular frente a los no mutados lo que podría indicar una relación entre la presencia del alelo A en niños obesos y niveles mayores de grasa subcutánea (AU)


OBJECTIVE: In the present study, our objectives were to evaluate the prevalence of -866G/A mutation of UCP2 gene and to study its influence on the phenotype of obese children (11-12 years old) from Navarra. BACKGROUND AND STUDY SETTING: Obesity is a disease with a multifactorial origin that may related be to the presence of mutations and polymorphisms in several candidate genes. The gene of the uncoupling protein UCP2 is one of the most studied ones in relation to obesity because it seems to participate in body composition and several metabolic processes control. Three polymorphisms have been described for this gene: an insertion/ deletion of 45 nucleotides, a nucleotide change of guanine for adenine in -866 position, an another change that replaces alanine for valine at amino acid position 55. According to several studies, the -866G allele is related to an increased risk of developing obesity, although the results are contradictory about this association in the literature. SUBJECTS: The study was carried out on 125 obese children (52% male), aged 11-12 years, selected through the Pediatric Endocrinology Departments of Clínica Universitaria and Hospital Virgen del Camino of Pamplona (Spain), the reported results on this association are contradictory. INTERVENTIONS: After checking the inclusion criteria, anthropometrical data (weight, height, BMI, tricipitaland subscapular skinfolds) were taken, and the percentage of fat mass was measured by bioelectrical impedance. Besides, plasma levels of total cholesterol, glucose, insulin,and leptin were measured. DNA was extracted from white blood cells to determine the genotype by PCR technique followed by BstUI digestion and furthervisualization in agarose gel with 2% ethidium bromide. RESULTS: The genetic analysis revealed a 0.404 frequency of the allele A, with a percentage of individuals G/G, G/A, and A/A of 40.0%, 39.2%, and 20.8%, respectively. Carriers of the A allele had a significantly higher sum of tricipital and subscapular folds (p = 0.034). No significant differences between mutant and non-mutant subjects with regard to the studied biochemical variables were observed. CONCLUSIONS: Subjects carrying the polymorphism present higher values of tricipital and subscapular skinfolds as compared to non-mutant subjects, which may indicate a relationship between the presence of the A allele in obese children and higher amounts of subcutaneous fat (AU)


Assuntos
Masculino , Feminino , Criança , Humanos , Proteínas de Membrana Transportadoras/genética , Proteínas Mitocondriais/genética , Mutação , Obesidade/genética , Polimorfismo Genético , Fenótipo
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