RESUMO
Obesity exacerbates aging-induced adipose tissue dysfunction. This study aimed to investigate the effects of long-term exercise on inguinal white adipose tissue (iWAT) and interscapular brown adipose tissue (iBAT) of aged obese mice. Two-month-old female mice received a high-fat diet for 4 months. Then, six-month-old diet-induced obese animals were allocated to sedentarism (DIO) or to a long-term treadmill training (DIOEX) up to 18 months of age. In exercised mice, iWAT depot revealed more adaptability, with an increase in the expression of fatty acid oxidation genes (Cpt1a, Acox1), and an amelioration of the inflammatory status, with a favorable modulation of pro/antiinflammatory genes and lower macrophage infiltration. Additionally, iWAT of trained animals showed an increment in the expression of mitochondrial biogenesis (Pgc1a, Tfam, Nrf1), thermogenesis (Ucp1), and beige adipocytes genes (Cd137, Tbx1). In contrast, iBAT of aged obese mice was less responsive to exercise. Indeed, although an increase in functional brown adipocytes genes and proteins (Pgc1a, Prdm16 and UCP1) was observed, few changes were found on inflammation-related and fatty acid metabolism genes. The remodeling of iWAT and iBAT depots occurred along with an improvement in the HOMA index for insulin resistance and in glucose tolerance. In conclusion, long-term exercise effectively prevented the loss of iWAT and iBAT thermogenic properties during aging and obesity. In iWAT, the long-term exercise program also reduced the inflammatory status and stimulated a fat-oxidative gene profile. These exercise-induced adipose tissue adaptations could contribute to the beneficial effects on glucose homeostasis in aged obese mice. (AU)
Assuntos
Animais , Camundongos , Tecido Adiposo Marrom/metabolismo , Tecido Adiposo Branco/metabolismo , Ácidos Graxos/metabolismo , Glucose/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Obesos , Obesidade/metabolismo , Obesidade/terapia , Termogênese/genéticaRESUMO
Bile acids or its derivatives may influence non-alcoholic fatty liver disease development through multiple mechanisms. Intestinal L-cells secrete glucagon-like peptide-1 (GLP-1) and can be activated by bile acids (BA) influencing insulin resistance and hepatic steatosis development and progression. The aim of the present study was to assess the effects of cholic acid (CA) or ursodeoxycholic acid (UDCA) administration on portal and systemic levels of GLP-1 in genetically obese mice with established hepatic steatosis. Eight-week-old ob/ob mice were fed CA or UDCA during 4 weeks. Systemic and portal GLP-1 levels were measured as well as glucose tolerance test, serum and biliary parameters, hepatic triglyceride content, liver histology, and hepatic gene expression of relevant genes related to bile secretion. Eight-week-old ob/ob mice
Assuntos
Animais , Camundongos , Obesidade/fisiopatologia , Ácidos e Sais Biliares/farmacocinética , Fígado Gorduroso/fisiopatologia , Camundongos Obesos , Peptídeo 1 Semelhante ao Glucagon , Incretinas , Resistência à InsulinaRESUMO
No disponible
Assuntos
Animais , Adulto , Masculino , Feminino , Camundongos , Humanos , Helicobacter pylori , Resistência à Insulina , Expressão Gênica , Interleucina-6 , Infecções por Helicobacter , Adipócitos , Camundongos Knockout , Mediadores da Inflamação , Camundongos Obesos , Mutação , Obesidade , Antibacterianos , Carboidratos , Células Cultivadas , Diabetes Mellitus Experimental , Tecido Adiposo , Fígado , Insulina , Inflamação , Lipídeos , Genótipo , Fator de Necrose Tumoral alfa , Polimorfismo Genético , Diabetes Mellitus Tipo 2 , Ilhotas Pancreáticas , Polimorfismo GenéticoRESUMO
No disponible
Assuntos
Animais , Adulto , Masculino , Feminino , Camundongos , Humanos , Helicobacter pylori , Resistência à Insulina , Interleucina-6 , Infecções por Helicobacter , Expressão Gênica , Adipócitos , Camundongos Knockout , Mediadores da Inflamação , Camundongos Obesos , Mutação , Obesidade , Antibacterianos , Células Cultivadas , Carboidratos , Diabetes Mellitus Experimental , Tecido Adiposo , Lipídeos , Fígado , Insulina , Inflamação , Genótipo , Fator de Necrose Tumoral alfa , Polimorfismo Genético , Diabetes Mellitus Tipo 2 , Ilhotas Pancreáticas , Polimorfismo GenéticoRESUMO
El artículo revisa los diferentes ejes endocrinológicos en relación con los niveles plasmáticos de leptina del paciente obeso. Existe una hipótesis glucocorticoidea como causa de obesidad. Los niveles plasmáticos en humanos de leptina están elevados en el síndrome de Cushing y hay una respuesta secretora franca de leptina a la dexametasona. La obesidad altera la función reproductora tanto en el hombre como en la mujer. Los niveles de leptina son mayores en la mujer que en el hombre y se requiere un nivel crítico de leptina en plasma para desarrollar la capacidad reproductora femenina. La interrelación entre el índice de masa corporal y los niveles circulantes de leptina varían en el curso de los ciclos ováricos, la mejor correlación aparece en la fase luteal, cuando los niveles de leptina y progesterona están mas altos. La obesidad se asocia a disminución de los niveles plasmáticos de GH, situación que revierte con la pérdida de peso. La infuliencia de la composición corporal sobre la secreción de GH en la obesidad puede estar relacionada con la leptina, que acutaría como una señal periférica del tejido adiposo. La disfución tiroidea no parece producir alteraciones en los niveles de leptina. Existe una interrelación significativa entre los niveles de insulina y leptina, pero ésta no está clara ya que en el paciente con diabetes tipo 2 encontramos niveles similares de leptina a los de los controles con similar indice de masa corporal (AU)
