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It is known that centrally injected ghrelin is an anorexigenic peptide in chicken. Its activity is not mediated by NPY/AgRP - producing neurons but through the corticosterone releasing hormone (CRH) - expressing neurons in hypothalamus which activate the hypothalamo-pituitary-adrenal (HPA) axis inducing an increase in plasma corticosterone levels. However, controversial results of peripheral ghrelin effect on appetite have been reported. Thus, the influence of intraperitoneal-injected ghrelin on the activity of the HPA axis in Cobb broiler chickens was examined. In addition, the effect of glucocorticoids antagonist (RU486) on the ghrelin activity was also investigated. The intraperitoneal co-injection of CRH-receptor antagonist, astressin, partially attenuated ghrelin-induced anorexia and corticosterone release. Co-administration of RU486 significantly enhanced the inhibitory effect of ghrelin on feed intake in 7-day- old broiler chickens. These results indicate that the peripheral ghrelin - induced anorexia is caused by the stimulation of HPA axis in chickens.
Ghrelin and obestatin are encoded by the same gene and originate from posttranslational processing of the preproghrelin peptide. The activities of ghrelin and obestatin are different. The effects of obestatin on feeding behavior, body weight regulation are the opposite to those of ghrelin. Administration of ghrelin increases food intake, while, contrarily, the systemic and central administration of obestatin inhibits feeding. Ghrelin and obestatin interact with two distinct subtypes of G-protein-coupled receptor: GHS-R and GPR 39
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Ghrelina - peptydowy hormon zoladkowy

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It is known that obesity is associated with a state of chronic low-level inflammation. Some data indicate that obesity- related stress could increase the hypothalamo-pituitary-adrenal axis activity. This leads to a rise in the plasma glucocorticoid level, which induces the development and differentiation of preadipocytes. Thus, the present study was performed to examine the effect of glucocorticoids on the expression of resistin and adiponectin mRNAs in adipose tissue during acute and chronic inflammation in mice. The results of the study showed an increase in the expression of resistin mRNA and a decrease in the expression of adiponectin mRNA during chronic inflammation (obese animals). Synthetic glucocorticoids changed the expression of both adipokines in a different manner according to the state of inflammation. To sum up, the action of glucocorticoids in adipose tissue depends on the immune system activity.
BACKGROUNDANDAIMS: The phenomenon of communication between the nervous and immune systems is commonly accepted. There were postulated several pathways for information exchange between these two systems, among them: neuronal with the vagus nerve, and enzymatic exercised through cyclooxygenases. The fact of biological compensation of many processes in our organisms is well known. In our project we hypothesized the existence of such phenomenon is situation of affected pathway for transferring of immune signal from the periphery to the brain after inhibition of cyclooxygenases. METHODS: To investigate the existence of these mechanisms, neurochemical changes occurring in the hypothalamus (the initial section of the stress axis – HPA) after intraperitoneal administration of LPS (10 mcg/animal) were analyzed. We studied the effect of long-term (10 days) administration of cyclooxygenases inhibitors on the neurochemical changes in the activity of the hypothalamus in response to LPS or saline ip administration. The rats were subcutaneously injected with selective cyclooxygenases inhibitors; Celecoxib (10 mg/kg) and SC-560 (3 mg/kg), respectively. RESULTS: Future HPLC analysis shown an increased activity of the noradrenergic and serotonergic systems within the hypothalamus. These data are comparable with those obtained after saline injections. CONCLUSIONS: These results suggest the presence of compensatory mechanisms responsible for the stimulation of the HPA axis after peripherally immune challenges. They also suggest that longterm intake of non-steroidal anti-inflammatory drugs may not affect, or in a very minor degree, the relationships between the immune and the nervous systems. Supported by NCN: UMO-2012/07/B/NZ4/00205.
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