Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
Medicina (Kaunas) ; 55(6)2019 Jun 19.
Artigo em Inglês | MEDLINE | ID: mdl-31248228

RESUMO

Background and objectives: Adipose tissue and skeletal muscle secrete adiponectin, a hormone abundantly secreted by adipocytes, that through the adiponectin receptor, regulate glucose and lipid metabolism. Adiponectin appears to protect skeletal muscles from inflammatory damage induced by oxidative stress. It has been suggested that decreased adiponectin levels could be associated with pathologic conditions, including obesity and diabetes. Furthermore, some studies suggest that exercise could have a beneficial effect by increasing adiponectin levels, but this observation remains controversial. It is also unknown if physical exercise modifies adiponectin expression in skeletal muscles. The aim of this study was to investigate the effect of chronic exercise on serum adiponectin and adiponectin expression in slow-twitch (soleus) and fast-twitch (plantaris) muscles in healthy rats. Materials and methods: Two-month-old male Wistar rats were randomly divided into three groups with n = 6 in each group: control (C), moderate-intensity training (MIT), and high-intensity training (HIT). The rats were conditioned to run on a treadmill for the 8-week period. Forty-eight hours after the last session, blood samples were collected for adiponectin measurements and total RNA was isolated from plantaris and soleus muscles to measure by RT-qPCR adiponectin receptor 1 and adiponectin mRNA expression level. Results: MIT and HIT groups had reduced adiponectin protein levels in serum and the plantaris muscle, but not changes in adiponectin protein were observed in the soleus muscle. No significant differences in Adiponectin receptor 1 (AdipoR1) gene expression were observed following intense or moderate exercise in either muscle group studied. Conclusions: Our study shows that decreasing levels of circulating adiponectin is a result of physical exercise and should not be generalized as a predictive marker of disease.


Assuntos
Adiponectina/análise , Músculo Esquelético/patologia , Condicionamento Físico Animal/fisiologia , Adiponectina/sangue , Análise de Variância , Animais , Modelos Animais de Doenças , Masculino , Músculo Esquelético/fisiologia , RNA/análise , RNA/sangue , Ratos , Ratos Wistar/sangue
2.
Rev. cuba. invest. bioméd ; 28(4)oct.-dic. 2009.
Artigo em Espanhol | LILACS | ID: lil-616446

RESUMO

Se ha descrito que el núcleo del tracto solitario (NTS), estructura del tallo cerebral y vía de relevo de las aferencias del los quimiorreceptores del senocuerpo carotídeo (RSCC), participa en el aumento en la retención de glucosa por el cerebro (RGC) ante una hipoxia. Es probable que en esta respuesta participe el óxido nítrico (NO) y la proteína Fos. En este trabajo se analiza el papel del NO en el NTS sobre la modificación de la RGC y la expresión de la proteína inmunorreactiva Fos (Fos-ir) en ratas in vivo. La inyección de un donador del NO como es el nitroprusiato de sodio (NPS) en el NTS, 4 min antes de la estimulación de los RSCC, disminuyó la RGC, pero incrementó la expresión de Fos-ir en un mayor número de neuronas en el NTS con respecto a las ratas control, que sólo recibieron líquido cefalorraquídeo artificial (LCRa) antes de la estimulación RSCC. En contraste, un inhibidor selectivo del NO como el N?-nitro-L-arginina metil éster (L-NAME) en el NTS 4 min antes de la estimulación RSCC con NaCN, aumentó la RGC, pero disminuyó el número de neuronas Fos-ir comparados con el control o con NPS. La detección inmunohistoquímica de la expresión de Fos-ir en las células del tallo cerebral indica que la estimulación RSCC activa vías dependientes de NO en el NTS, para regular la RGC. El estudio de esta población de células en el NTS, serß importante para definir su caracterización.


It has been said that the nucleus tractus solitarii (NTS), one structure of the brain stem and path of apherences of chemoreceptors of carotid sinus-body, is involved in the increased glucose retention by the brain in case of hypoxia. It is likely that nitric oxide and Fos protein also take part in this response. This paper analyzes the role of nitric oxide in the NTS on the change of glucose retention by the brain and the expression of inmunoreactive protein Fos (ir-Fos) in rats in vivo. The injection of a NO donor such as sodium nitroprusiate in the NTS four minutes before the stimulation of carotid sinus-body chemoreceptors decreased glucose retention by the brain but increased the expression of ir-Fos in a higher number of neurons in NTS with respect to control group rats which only received artificial cerebrospinal fluid before the stimulation. In contrast, the use of a selective NO inhibitor such as NO-nitro-L-arginine methyl ester (L-NAME) in the NTS four minutes before the stimulation of the chemoreceptors with NaCN, increased the glucose retention by the brain but reduced the number of neurons with ir-Fos expression when compared with the control group or the sodium nitroprusiate injection. The immunohistochemical detection of ir-Fos expression in the brain stem cells indicated that stimulation of carotid sinus-body chemoreceptors activated NO-dependent paths in the NTS to regulate glucose retention by the brain. The study of this cell population in the NTS will be important to define its characterization.


Assuntos
Animais , Ratos , Hipóxia/patologia , Glucose , Óxido Nítrico/análise , Tronco Encefálico/fisiopatologia
3.
Rev. cuba. invest. bioméd ; 28(4)oct.-dic. 2009.
Artigo em Espanhol | CUMED | ID: cum-45348

RESUMO

Se ha descrito que el núcleo del tracto solitario (NTS), estructura del tallo cerebral y vía de relevo de las aferencias del los quimiorreceptores del senocuerpo carotídeo (RSCC), participa en el aumento en la retención de glucosa por el cerebro (RGC) ante una hipoxia. Es probable que en esta respuesta participe el óxido nítrico (NO) y la proteína Fos. En este trabajo se analiza el papel del NO en el NTS sobre la modificación de la RGC y la expresión de la proteína inmunorreactiva Fos (Fos-ir) en ratas in vivo. La inyección de un donador del NO como es el nitroprusiato de sodio (NPS) en el NTS, 4 min antes de la estimulación de los RSCC, disminuyó la RGC, pero incrementó la expresión de Fos-ir en un mayor número de neuronas en el NTS con respecto a las ratas control, que sólo recibieron líquido cefalorraquídeo artificial (LCRa) antes de la estimulación RSCC. En contraste, un inhibidor selectivo del NO como el N?-nitro-L-arginina metil éster (L-NAME) en el NTS 4 min antes de la estimulación RSCC con NaCN, aumentó la RGC, pero disminuyó el número de neuronas Fos-ir comparados con el control o con NPS. La detección inmunohistoquímica de la expresión de Fos-ir en las células del tallo cerebral indica que la estimulación RSCC activa vías dependientes de NO en el NTS, para regular la RGC. El estudio de esta población de células en el NTS, serß importante para definir su caracterización(AU)


It has been said that the nucleus tractus solitarii (NTS), one structure of the brain stem and path of apherences of chemoreceptors of carotid sinus-body, is involved in the increased glucose retention by the brain in case of hypoxia. It is likely that nitric oxide and Fos protein also take part in this response. This paper analyzes the role of nitric oxide in the NTS on the change of glucose retention by the brain and the expression of inmunoreactive protein Fos (ir-Fos) in rats in vivo. The injection of a NO donor such as sodium nitroprusiate in the NTS four minutes before the stimulation of carotid sinus-body chemoreceptors decreased glucose retention by the brain but increased the expression of ir-Fos in a higher number of neurons in NTS with respect to control group rats which only received artificial cerebrospinal fluid before the stimulation. In contrast, the use of a selective NO inhibitor such as NO-nitro-L-arginine methyl ester (L-NAME) in the NTS four minutes before the stimulation of the chemoreceptors with NaCN, increased the glucose retention by the brain but reduced the number of neurons with ir-Fos expression when compared with the control group or the sodium nitroprusiate injection. The immunohistochemical detection of ir-Fos expression in the brain stem cells indicated that stimulation of carotid sinus-body chemoreceptors activated NO-dependent paths in the NTS to regulate glucose retention by the brain. The study of this cell population in the NTS will be important to define its characterization(AU)


Assuntos
Animais , Ratos , Óxido Nítrico/análise , Glucose , Tronco Encefálico/fisiopatologia , Hipóxia/patologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...