Base de datos : IBECS
Búsqueda : "1138-7548" [ISSN]
Referencias encontradas : 694 [refinar]
Mostrando: 1 .. 10   en el formato [Detallado]

página 1 de 70 va a la página                         

  1 / 694 IBECS  
              next record last record
selecciona
para imprimir
Id: 168487
Autor: Alrob, Osama Abo; Khatib, Said; Naser, Saleh A.
Título: MicroRNAs 33, 122, and 208: a potential novel targets in the treatment of obesity, diabetes, and heart-related diseases
Fuente: J. physiol. biochem;73(2):307-314, mayo 2017. ilus, tab.
Idioma: en.
doi: 10.1007/s13105-016-0543-z.
Resumen: Despite decades of research, obesity and diabetes remain major health problems in the USA and worldwide. Among the many complications associated with diabetes is an increased risk of cardiovascular diseases, including myocardial infarction and heart failure. Recently, microRNAs have emerged as important players in heart disease and energy regulation. However, little work has investigated the role of microRNAs in cardiac energy regulation. Both human and animal studies have reported a significant increase in circulating free fatty acids and triacylglycerol, increased cardiac reliance on fatty acid oxidation, and subsequent decrease in glucose oxidation which all contributes to insulin resistance and lipotoxicity seen in obesity and diabetes. Importantly, MED13 was initially identified as a negative regulator of lipid accumulation in Drosophilia. Various metabolic genes were downregulated in MED13 transgenic heart, including sterol regulatory element-binding protein. Moreover, miR-33 and miR-122 have recently revealed as key regulators of lipid metabolism. In this review, we will focus on the role of microRNAs in regulation of cardiac and total body energy metabolism. We will also discuss the pharmacological and non-pharmacological interventions that target microRNAs for the treatment of obesity and diabetes (AU)

No disponible
Descriptores: obesidad/metabolismo
modelos biológicos
microARN/metabolismo
enfermedades cardíacas/metabolismo
diabetes mellitus/metabolismo
-cardiotónicos/uso terapéutico
fármacos antiobesidad/uso terapéutico
regulación de la expresión génica/efectos de drogas
hipoglicemiantes/uso terapéutico
metabolismo lipídico/efectos de drogas
diseño de fármacos
metabolismo energético/efectos de drogas
terapia molecular selectiva
Límites: humanos
animales
Tipo de Publicación: revisión
Responsable: BNCS


  2 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168486
Autor: Grzelak, Teresa; Dutkiewicz, Agata; Paszynska, Elzbieta; Dmitrzak-Weglarz, Monika; Slopien, Agnieszka; Tyszkiewicz-Nwafor, Marta.
Título: Neurobiochemical and psychological factors influencing the eating behaviors and attitudes in anorexia nervosa
Fuente: J. physiol. biochem;73(2):297-305, mayo 2017.
Idioma: en.
doi: 10.1007/s13105-016-0540-2.
Resumen: The aim of this study was to determine the characteristic features which contribute to inappropriate eating attitudes in people suffering from anorexia nervosa, based on an analysis of recent data. Factors influencing these attitudes have a genetic, neurobiological, biochemical, affective-motivational, cognitive, and behavioral background. Another important issue addressed in the paper is a description of the mechanism leading to continuous dietary restrictions. The altered activity of neurotransmitters modulating patients' moods after the consumption of food and a disturbed responsiveness to enterohormones enhance affective-motivational and cognitive aspects which, in turn, impede the improvement of eating behaviors. An understanding of the mechanisms behind the factors affecting the maintenance of inappropriate eating attitudes may contribute to greater effectiveness in the treatment of anorexia nervosa (AU)

No disponible
Descriptores: anorexia nerviosa/fisiopatología
modelos psicológicos
conducta alimentaria/psicología
actitud ante la salud
conocimientos, actitudes y prácticas sanitarias
-tratamiento combinado
disfunción cognitiva
motivación
trastorno obsesivo compulsivo
fenómenos fisiológicos del sistema nervioso
medicina de precisión
Límites: humanos
animales
Tipo de Publicación: revisión
Responsable: BNCS


  3 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168485
Autor: Ren, Kun; Lu, Yan-Jun; Mo, Zhong-Cheng; Liu, Xing; Tang, Zhen-Li; Jiang, Yue; Peng, Xiao-Shang; Li, Li; Zhang, Qing-Hai; Yi, Guang-Hui.
Título: ApoA-I/SR-BI modulates S1P/S1PR2-mediated inflammation through the PI3K/Akt signaling pathway in HUVECs
Fuente: J. physiol. biochem;73(2):287-296, mayo 2017. graf, ilus.
Idioma: en.
doi: 10.1007/s13105-016-0553-5.
Resumen: Endothelial dysfunction plays a vital role during the initial stage of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) induces vascular endothelial injury and vessel wall inflammation. Sphingosine-1-phosphate (S1P) exerts numerous vasoprotective effects by binding to diverse S1P receptors (S1PRs; S1PR1-5). A number of studies have shown that in endothelial cells (ECs), S1PR2 acts as a pro-atherosclerotic mediator by stimulating vessel wall inflammation through the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Scavenger receptor class B member I (SR-BI), a high-affinity receptor for apolipoprotein A-I (apoA-I)/high-density lipoprotein (HDL), inhibits nuclear factor-κB (NF-κB) translocation and decreases the plasma levels of inflammatory mediators via the PI3K/Akt pathway. We hypothesized that the inflammatory effects of S1P/S1PR2 on ECs may be regulated by apoA-I/SR-BI. The results showed that ox-LDL, a pro-inflammatory factor, augmented the S1PR2 level in human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner. In addition, S1P/S1PR2 signaling influenced the levels of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10, aggravating inflammation in HUVECs. Moreover, the pro-inflammatory effects induced by S1P/S1PR2 were attenuated by SR-BI overexpression and enhanced by an SR-BI inhibitor, BLT-1. Further experiments showed that the PI3K/Akt signaling pathway was involved in this process. Taken together, these results demonstrate that apoA-I/SR-BI negatively regulates S1P/S1PR2-mediated inflammation in HUVECs by activating the PI3K/Akt signaling pathway (AU)

No disponible
Descriptores: endotelio vascular/metabolismo
lisofosfolípidos/metabolismo
receptores depuradores de clase B/agonistas
receptores de lisoesfingolípidos/agonistas
esfingosina/análogos & derivados
transducción de señales/efectos de drogas
fosfatidil inositol 3 cinasas/metabolismo
-regulación de la expresión génica/efectos de drogas
transporte activo del núcleo celular/efectos de drogas
ciclopentanos/farmacología
tiosemicarbazonas/farmacología
factor de necrosis tumoral alfa
células endoteliales de la vena umbilical humana
lipoproteínas LDL
proteínas protooncogénicas c-akt
Límites: humanos
Responsable: BNCS


  4 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168484
Autor: Campisano, Sabrna Edith; Echarte, Stella Maris; Podaza, Enrique; Chisari, Andrea Nancy.
Título: Protein malnutrition during fetal programming induces fatty liver in adult male offspring rats
Fuente: J. physiol. biochem;73(2):275-285, mayo 2017. tab, ilus, graf.
Idioma: en.
doi: 10.1007/s13105-016-0549-1.
Resumen: We evaluated the effects of protein malnutrition on liver morphology and physiology in rats subjected to different malnutrition schemes. Pregnant rats were fed with a control diet or a low protein diet (LPD). Male offspring rats received a LPD during gestation, lactation, and until they were 60 days old (MM group), a late LPD that began after weaning (CM), or a LPD administrated only during the gestation-lactation period followed by a control diet (MC). On day 60, blood was collected and the liver was dissected out. We found a decrease in MM rats' total body (p < 0.001) and liver (p < 0.05) weight. These and CM rats showed obvious liver dysfunction reflected by the increase in serum glutamic pyruvic transaminase (SGOT) (MM p < 0.001) and serum glutamic pyruvic transaminase (SGPT) (MM and CM p < 0.001) enzymes, and liver content of cholesterol (MM and CM p < 0.001) and triglycerides (MM p < 0.01; CM p < 0.001), in addition to what we saw by histology. Liver dysfunction was also shown by the increase in gamma glutamyl transferase (GGT) (MM, MC, and CM p < 0.001) and GST-pi1 (MM and CM p < 0.001, MC p < 0.05) expression levels. MC rats showed the lowest increment in GST-pi1 expression (MC vs. MM; p < 0.001, MC vs. CM; p < 0.01). ROS production (MM, CM, and MC: p < 0.001), lipid peroxidation (MM, CM, and MC p < 0.001), content of carbonyl groups in liver proteins (MM and CM p < 0.001, MC p < 0.01), and total antioxidant capacity (MM, CM, and MC p < 0.001) were increased in the liver of all groups of malnourished animals. However, MM rats showed the highest increment. We found higher TNF-α (MM and CM p < 0.001), and IL-6 (MM and CM p < 0.001) serum levels and TGF-β liver content (MM p < 0.01; CM p < 0.05), in MM and CM groups, while MC rats reverted the values to normal levels. Pro-survival signaling pathways mediated by tyrosine or serine/threonine kinases (pAKT) (MM and CM p < 0.001; MC p < 0.01) and extrasellular signal-regulated kinase (pERKs) (MM p < 0.01; CM p < 0.05) appeared to be activated in the liver of all groups of malnourished rats, suggesting the presence of cells resistant to apoptosis which would become cancerous. In conclusion, a LPD induced liver damage whose magnitude was related to the developmental stage at which malnutrition occurs and to its length (AU)

No disponible
Descriptores: desarrollo fetal
lactancia
hígado/fisiopatología
estrés oxidativo
dieta restrictiva en proteínas/efectos adversos
fenómenos fisiológicos nutricionales maternos
esteatosis hepática no alcohólica/etiología
-biomarcadores/sangre
citocinas/metabolismo
regulación de la expresión génica
peroxidación de lípidos
distribución aleatoria
ratas Wistar
aumento de peso
hiperlipidemias/etiología
especies reactivas de oxígeno
carbonilación proteica
Límites: animales
masculino
femenino
embarazo
Tipo de Publicación: estudio comparativo
Responsable: BNCS


  5 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168483
Autor: Reed, Dustin K; Carter, Anthony; Dixit, Mehul; Arany, Istvan.
Título: p66shc-mediated toxicity of high-dose alfa-tocopherol in renal proximal tubule cells
Fuente: J. physiol. biochem;73(2):267-273, mayo 2017.
Idioma: en.
doi: 10.1007/s13105-016-0551-7.
Resumen: α-Tocopherol (TOC) is a widely used supplement known for its role as an antioxidant. Previously, we have shown that TOC elicits adaptive responses by upregulating the ERK/CREB/HO-1 pathway, which depends on its concentration in cultured renal proximal tubule cells (RPTCs). This suggests that high-dose TOC (hTOC) may elicit adverse effects via inflicting oxidative stress. Since the pro-oxidant p66shc is a major mediator of oxidant injury in various models of renal toxicants, we tested the hypothesis that hTOC elicits renal toxicity through activation of p66shc and consequent oxidative stress. RPTCs (NRK52E) were treated with high-dose TOC (hTOC; 400 nM) in cells where expression or mitochondrial cytochrome c-binding of p66shc was manipulated by genetic means. Intracellular production of reactive oxygen species (ROS), mitochondrial depolarization, and cell viability was also determined. Additionally, activation of the pro-survival ERK/CREB/HO-1 signaling and the p66shc promoter was determined via reporter luciferase assays. hTOC decreased cell viability via increasing ROS-dependent mitochondrial depolarization and suppressing the pro-survival ERK/CREB/HO-1 pathway via transcriptional activation of p66shc. Conversely, either knockdown of p66shc, mutation of its mitochondrial cytochrome c-binding site, or overexpression of ERK or HO-1 ameliorated adverse effects of hTOC and restored the pro-survival signaling. The pro-oxidant p66shc plays dual role in toxicity of high-dose TOC: it provokes oxidative stress and suppresses adaptive responses (AU)

No disponible
Descriptores: antioxidantes/efectos adversos
túbulos renales proximales/metabolismo
regulación de la expresión génica
estrés oxidativo
proteína transformadora 1 que contiene dominios de homología 2 de Src/metabolismo
alfa-tocoferol/efectos adversos
-sustitución de aminoácidos
suplementos dietéticos/efectos adversos
potencial de membrana mitocondrial
sistema de señalización de las MAP cinasas
proteínas de fusión recombinantes
especies reactivas de oxígeno
técnicas de silenciamiento génico
citocromos c
sitios de unión
Límites: animales
ratas
Responsable: BNCS


  6 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168482
Autor: Zhou, Yuanyuan; Li, Chaoyan; Li, Deheng; Zheng, Yapng; Wang, Jin.
Título: IL-5 blocks apoptosis and tau hyperphosphorylation induced by Abeta25-35 peptide in PC12 cells
Fuente: J. physiol. biochem;73(2):259-266, mayo 2017. graf.
Idioma: en.
doi: 10.1007/s13105-016-0550-8.
Resumen: The primary features of Alzheimer's disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid β (Aβ) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aβ25-35-induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aβ25-35-evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling (AU)

No disponible
Descriptores: neuronas/metabolismo
interleucina-5/metabolismo
apoptosis/efectos de drogas
péptidos beta amiloides/metabolismo
subunidad alfa del receptor de interleucina-5/agonistas
proteínas tau/metabolismo
procesamiento postraduccional de las proteínas/efectos de drogas
-enfermedad de Alzheimer
sulfonamidas/farmacología
supervivencia celular/efectos de drogas
activación enzimática/efectos de drogas
cinasa Janus 2
proteínas del tejido nervioso
células PC12
pirrolidinas/farmacología
interferencia por ARN
inhibidores de proteínas cinasas/farmacología
Límites: animales
ratas
Responsable: BNCS


  7 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168481
Autor: Lara-Diaz, VJ; Castilla-Cortazar, I; Martín-Estal, I; García-Magariño, M; Aguirre, GA; Puche, JE; Garza, RG de la; Morales, LA; Muñoz, U.
Título: IGF-1 modulates gene expression of proteins involved in inflammation, cytoskeleton, and liver architecture
Fuente: J. physiol. biochem;73(2):245-258, mayo 2017. ilus, tab, graf.
Idioma: en.
doi: 10.1007/s13105-016-0545-x.
Resumen: Even though the liver synthesizes most of circulating IGF-1, it lacks its receptor under physiological conditions. However, according to previous studies, a damaged liver expresses the receptor. For this reason, herein, we examine hepatic histology and expression of genes encoding proteins of the cytoskeleton, extracellular matrix, and cell-cell molecules and inflammation-related proteins. A partial IGF-1 deficiency murine model was used to investigate IGF-1's effects on liver by comparing wild-type controls, heterozygous igf1+/-, and heterozygous mice treated with IGF-1 for 10 days. Histology, microarray for mRNA gene expression, RT-qPCR, and lipid peroxidation were assessed. Microarray analyses revealed significant underexpression of igf1 in heterozygous mice compared to control mice, restoring normal liver expression after treatment, which then normalized its circulating levels. IGF-1 receptor mRNA was overexpressed in Hz mice liver, while treated mice displayed a similar expression to that of the controls. Heterozygous mice showed overexpression of several genes encoding proteins related to inflammatory and acute-phase proteins and underexpression or overexpression of genes which coded for extracellular matrix, cytoskeleton, and cell junction components. Histology revealed an altered hepatic architecture. In addition, liver oxidative damage was found increased in the heterozygous group. The mere IGF-1 partial deficiency is associated with relevant alterations of the hepatic architecture and expression of genes involved in cytoskeleton, hepatocyte polarity, cell junctions, and extracellular matrix proteins. Moreover, it induces hepatic expression of the IGF-1 receptor and elevated acute-phase and inflammation mediators, which all resulted in liver oxidative damage (AU)

No disponible
Descriptores: regulación de la expresión génica
hepatitis/metabolismo
receptores de somatomedinas/metabolismo
proteínas de fase aguda/metabolismo
mediadores de la inflamación/metabolismo
factor I de crecimiento insulinoide/metabolismo
hígado/metabolismo
-estrés oxidativo
cadherinas
desmosomas
peroxidación de lípidos
inyecciones subcutáneas
hibridación genética
proteínas de las uniones estrechas
proteínas de la matriz extracelular
perfiles de expresión génica
ratones transgénicos
Límites: animales
masculino
ratones
Tipo de Publicación: estudio comparativo
Responsable: BNCS


  8 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168480
Autor: García, José Antonio; Ortiz, Francisco; Miana, Javier; Doerrier, Carolina; Fernández-Ortiz, Marisol; Rusanova, Iryna; Escames, Germaine; García, José Joaquín; Acuña-Castroviejo, Darío.
Título: Contribution of inducible and neuronal nitric oxide synthases to mitochondrial damage and melatonin rescue in LPS-treated mice
Fuente: J. physiol. biochem;73(2):235-244, mayo 2017. graf.
Idioma: en.
doi: 10.1007/s13105-016-0548-2.
Resumen: NOS isoform activation is related to liver failure during sepsis, but the mechanisms driving mitochondrial impairment remain unclear. We induced sepsis by LPS administration to inducible nitric oxide synthase (iNOS-/-) and neuronal nitric oxide synthase (nNOS-/-) mice and their respective wild-type controls to examine the contribution of iNOS to mitochondrial failure in the absence of nNOS. To achieve this goal, the determination of messenger RNA (mRNA) expression and protein content of iNOS in cytosol and mitochondria, the mitochondrial respiratory complex content, and the levels of nitrosative and oxidative stress (by measuring 3-nitrotyrosine residues and carbonyl groups, respectively) were examined in the liver of control and septic mice. We detected strongly elevated iNOS mRNA expression and protein levels in liver cytosol and mitochondria of septic mice, which were related to enhanced oxidative and nitrosative stress, and with fewer changes in respiratory complexes. The absence of the iNOS, but not nNOS, gene absolutely prevented mitochondrial impairment during sepsis. Moreover, the nNOS gene did not modify the expression and the effects of iNOS here shown. Melatonin administration counteracted iNOS activation and mitochondrial damage and enhanced the expression of the respiratory complexes above the control values. These effects were unrelated to the presence or absence of nNOS. iNOS is a main target to prevent liver mitochondrial impairment during sepsis, and melatonin represents an efficient antagonist of these iNOS-dependent effects whereas it may boost mitochondrial respiration to enhance liver survival (AU)

No disponible
Descriptores: antioxidantes/uso terapéutico
modelos de enfermedad en animales
insuficiencia hepática/prevención & control
hígado/efectos de drogas
melatonina/uso terapéutico
sepsis/tratamiento farmacológico
óxido nítrico sintasa de tipo II/metabolismo
-óxido nítrico sintasa de tipo I
regulación de la expresión génica enzimológica/efectos de drogas
lipopolisacáridos/toxicidad
biomarcadores/sangre
carbonilación proteica/efectos de drogas
mitocondrias hepáticas
ARN mensajero/metabolismo
estrés oxidativo/efectos de drogas
inyecciones intraperitoneales
Límites: animales
ratones
Tipo de Publicación: estudio comparativo
Responsable: BNCS


  9 / 694 IBECS  
              first record previous record next record last record
selecciona
para imprimir
Id: 168479
Autor: Labayen, Idoia; Ruiz, Jonatan R; Huybrechts, Inge; Ortega, Francisco B; Castillo, Manuel; Sjöstrom, Michael; González-Gross, Marcela; Manios, Yannis; Widhalm, Kurt; Kafatos, Anthony; Breidenassel, Christina; Rodríguez, Gerardo; Dallongeville, Jean; Gottrand, Frédéric; Moreno, Luis A.
Título: Ideal cardiovascular health and liver enzyme levels in European adolescents; the HELENA study
Fuente: J. physiol. biochem;73(2):225-234, mayo 2017. tab, graf.
Idioma: en.
doi: 10.1007/s13105-016-0546-9.
Resumen: There is an increasing interest for the role of liver enzymes as predictors of non-liver-related morbidity and mortality. The American Heart Association (AHA) described the ideal cardiovascular health concept as a score of seven cardiovascular health behaviors and factors that can be used to monitor and predict ideal cardiovascular health over time. This study aimed to examine the association of the ideal cardiovascular health (ICH), as defined by the AHA, with liver enzyme levels in European adolescents. A total of 637 adolescents (54.6% females), aged 14.6 ± 1.2 years from nine European countries participated in this cross-sectional study. Blood levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase were measured and the AST/ALT ratio calculated. Ideal cardiovascular health was defined as meeting ideal levels of the following components: four behaviors (smoking, body mass index, physical activity, and diet) and three factors (total cholesterol, blood pressure, and glucose). A higher number of ideal cardiovascular health behaviors, factors, and ideal cardiovascular health index were associated with lower ALT (P < 0.05, P < 0.001, and P < 0.001, respectively) and gamma-glutamyltransferase (P < 0.001, P < 0.01, and P < 0.001, respectively) levels. Similarly, a higher number of ideal cardiovascular health behaviors (P < 0.01), factors (P < 0.01), and ideal cardiovascular health index (P < 0.001) were associated with a higher aspartate aminotransferase to alanine aminotransferase ratio. These findings reinforce the usefulness of the ICH index as an instrument to identify target individuals and promote cardiovascular health in adolescents, and it also extends these observations to the liver manifestation of the metabolic síndrome (AU)

No disponible
Descriptores: salud del adolescente/etnología
fenómenos fisiológicos cardiovasculares
estilo de vida saludable
estado de salud
hígado/fisiología
salud urbana/etnología
-factores de riesgo
valores de referencia
prevalencia
obesidad pediátrica
biomarcadores/sangre
estudios de cohortes
Europa (continente)/epidemiología
índice de masa corporal
Límites: humanos
masculino
femenino
adolescente
Tipo de Publicación: estudio comparativo
Responsable: BNCS


  10 / 694 IBECS  
              first record previous record
selecciona
para imprimir
Id: 168478
Autor: Kocher, Caitlin; Christiansen, Matthew; Martin, Sarah; Adams, Christopher; Wehner, Paulette; Gress, Todd; Santanam, Nalini.
Título: Sexual dimorphism in obesity-related genes in the epicardial fat during aging
Fuente: J. physiol. biochem;73(2):215-224, mayo 2017. tab, ilus, graf.
Idioma: en.
doi: 10.1007/s13105-016-0542-0.
Resumen: Aging increases the risk of cardiovascular disease and metabolic syndrome. Alterations in epicardial fat play an important pathophysiological role in coronary artery disease and hypertension. We investigated the impact of normal aging on obesity-related genes in epicardial fat. Sex-specific changes in obesity-related genes with aging in epicardial fat (EF) were determined in young (6 months) and old (30/36 months) female and male, Fischer 344 × Brown Norway hybrid (FBN) rats, using a rat obesity RT2 PCR Array. Circulating sex hormone levels, body and heart weights were determined. Statistical significance was determined using two-tailed Student's t test and Pearson's correlation. Our results revealed sex-specific differences in obesity-related genes with aging. Dramatic changes in the expression profile of obesity-related genes in EF with aging in female, but not in male, FBN rats were observed. The older (30 months) female rats had more significant variations in the abundance of obesity-related genes in the EF compared to that seen in younger female rats or both age groups in male rats. A correlation of changes in obesity-related genes in EF to heart weights was observed in female rats, but not in male rats with aging. No correlation was observed to circulating sex hormone levels. Our findings indicate a dysfunctional EF in female rats with aging compared to male rats. These findings, with further functional validation, might help explain the sex differences in cardiovascular risk and mortality associated with aging observed in humans (AU)

No disponible
Descriptores: tejido adiposo blanco/metabolismo
adiposidad
envejecimiento
enfermedad arterial coronaria/etiología
hipertensión/etiología
obesidad/genética
regulación de la expresión génica en el desarrollo
-perfiles de expresión génica
cruzamientos genéticos
miocardio/patología
pericardio
aumento de peso
características sexuales
ratas consanguíneas BN
ratas consanguíneas F344
Límites: animales
masculino
femenino
ratas
Tipo de Publicación: estudios de validación
Responsable: BNCS



página 1 de 70 va a la página                         
   


Refinar la búsqueda
  Base de datos : IBECS Formulario avanzado   
Buscar por : Formulario libre    Formulario básico

    Buscar en el campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPS/OMS - Centro Latinoamericano y del Caribe de Información en Ciencias de la Salud