Endocrine Abstracts

Ghrelin is protein hormone originally isolated from the stomach and it is the endogenous ligand for the growth hormone secretagogue receptor (GSH-R 1a). It is well established that ghrelin plays roles in appetite regulation, gut function, metabolic disorders and inflammation. Ghrelin and its receptor is expressed in brain and peripheral tissues sensitive to inflammation such as heart and spleen. As a part of study dealing with the role of ghrelin in the development of inflammation the present study was carried out to assess the effect of streptozotocin (inflammatory agent) on the ghrelin concentration, expression of ghrelin and its receptor genes in piglets heart and spleen. Animal studies were performed on 6 weeks old piglets divided into control and experimental group treated with streptozotocin (STZ) 3 times every two days (75+50+25 mg, i.p.). Ghrelin concentration was estimated by RIA, expression of genes of ghrelin (ghrl) and its receptor (GHS-R1a) was measured by PCR-RT. Expression of ghrelin receptor protein was estimated by Western blot analysis. All tested parameters were higher in the heart than in spleen of control animals. Streptozotocin injections significantly increased the expression of ghrelin and its receptor genes as well as the receptor protein concentration in heart - by 7, 5 and 2 times, respectively. However, the concentration of ghrelin in piglets treated with STZ was lower in the heart and higher in the spleen. Unexpectedly, in spite of higher level of ghrelin receptor protein the expression of ghrelin gene was decreased in the spleen of STZ treated piglets.

The obtained results clearly showed that inflammation and diabetes type I induced by STZ changed the activity of the ghrelin-receptor system in the heart and spleen of piglets. The expression of ghrelin and its functional receptor genes was tissue specific.

Study was supported by NCBiR grant NR 12 0064 06.

Declaration of interest.: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.