OBJECTIVETo investigate effects of in ovo ghrelin administration on serum malondialdehyde (MDA) level in newly-hatched chickens.

METHODSFertilized eggs were divided into 7 groups: group T1 as control (without injection), group T2 (in ovo injected with 50 ng/egg ghrelin on day 5), group T3 (in ovo injected with 100 ng/egg ghrelin on day 5), group T4 (in ovo injected with 50 ng/egg ghrelin on day 10), group T5 (in ovo injected with 100 ng/egg ghrelin on day 10), group T6 (in ovo injected with solvent: 1% acetic acid, without ghrelin on day 5) and group T7 (in ovo injected with solvent without ghrelin on day 10). After hatching, serum MDA concentrations were determined.

RESULTSGhrelin administrated groups (T2, T3, T4 and T5) had lower serum MDA level in comparison with control group (T1) or solvent injected groups (T6 and T7). T2 and T3 (ghrelin injection on day 5) had significantly lower MDA concentrations (4.10 and 4.60 nmol/mL, respectively) in comparison with other groups. In T4 and T5, MDA levels were lower than T1, T6 and T7 (non-ghrelin administrated groups) (9.53 and 9.50 in comparison with 10.73, 10.03 and 10.13 nmol/mL) and were higher than T2 and T3.

CONCLUSIONSIt can be concluded that in ovo administration of ghrelin can have anti-oxidative protection and reduce serum MDA level. Ghrelin administration on day 5 of incubation is more efficient.

Animals ; Antioxidants ; administration & dosage ; Chickens ; Ghrelin ; administration & dosage ; Malondialdehyde ; blood ; Serum ; chemistry

Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-KappaB (NF-KappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.
Amino Acid Sequence ; Appetite Stimulants ; Gastritis/*metabolism/microbiology ; Ghrelin/*blood/chemistry ; Helicobacter Infections/*metabolism ; *Helicobacter pylori ; Humans ; Insulin-Like Growth Factor I/analysis ; Leptin/*blood ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Neurosecretory Systems/*metabolism ; Peptide Hormones/*blood ; Signal Transduction ; Weight Gain