Author(s): Zahra Farahani, Mahnaz Taherianfard and Saied Nazifi
Aim: Ethanol intake decreases food intake in rat, and one of the possible mediators of this alcohol effect is leptin. On the other hand, the concentration of total plasma homocysteine is a well-established indicator for the risk of cardiovascular disease, and seems to be related to ethanol consumption. So, the aim of the present study was to investigate the effect of exposure to acute (70%) and chronic (10%) evaporated ethanol on 1) brain leptin and homocysteine concentration on the 15th day of embryonic development of chick; 2) brain leptin and homocysteine concentration immediately after hatch of chick; 3) serum leptin concentration immediately after hatch of chick.
Methods: 60 fertilized eggs were used. Eggs were divided into 3 groups, 1) Control; 2) acute exposure to ethanol 3) chronic exposure to ethanol. Homocysteine was measured by using enzyme-linked assay, and leptin was measured with the chick leptin radioimmunoassay kit.
Results: Data showed that exposure to acute and chronic ethanol significantly (P<0.05) decreased brain homocysteine concentration on the 15th day of embryonic stage of chicken, but did not have any effect on brain homocysteine concentration immediately after hatch Exposure to acute and chronic ethanol significantly (P<0.05) increased brain leptin on the 15th day of embryonic stage, brain leptin immediately after hatch of chick and plasma leptin immediately after hatch of chick.
Conclusion: Present results indicated that exposure to acute and chronic ethanol by evaporation in embryonic stage of chicken can change the brain homocysteine, brain leptin and serum leptin.
