Effect of Niacin on Hyperleptinemia and Ob Gene mRNA Over-Expression in Adipose Tissue of Dexamethasone Treated Rats
Tahoora Shomali, Mahnaz Taherianfard, Mehdi Fazeli and Niloofar Safaei
DOI : 10.3844/ajptsp.2011.49.54
American Journal of Pharmacology and Toxicology
Volume 6, Issue 2
Problem statement: Glucocorticoid-induced ob gene over-expression and resulted hyperleptinemia may lead to adverse consequences especially on cardiovascular system; therefore, the present study was conducted to evaluate the effects of niacin on hyperleptinemia and ob gene over-expression due to dexamethasone administration in rats. Approach: Twenty four adult male rats divided randomly into four equal groups: (1) normal saline (control), (2) dexamathasone 0.125 mg kg-1 day-1, I.M. (3) dexamathasone 0.125 mg kg-1 day-1, I.M. + niacin 200 mg kg-1 day-1, by oral gavages and (4) niacin 200 mg kg-1 day-1, by oral gavages. After two weeks, blood samples were collected from all animals and leptin level assayed in harvested sera by ELISA method. Moreover, inguinal adipose tissue was excised to be examined for ob gene expression using quantitative real-time PCR. Results: Dexamethasone treatment (group 2) increased serum leptin along with its mRNA expression more than 3 folds as compared to control (p<0.001 and p = 0.001 respectively). Although leptin level in rats treated with dexamethasone+niacin was 17.8% lower than group 2; however this decrease was not significant (p>0.05). Concomitant administration of niacin with dexamethasone significantly decreased leptin gene mRNA expression compared to dexamethasone treated rats (p<0.001) and even reversed it to the control level (p>0.05). Niacin alone (group 4) had no effect on serum leptin concentration as well as leptin gene expression in comparison with control group (p>0.05). Conclusion: Niacin slightly ameliorates hyperleptinemia and reverses ob gene mRNA over-expression in adipose tissue of dexamethasone treated rats.
© 2011 Tahoora Shomali, Mahnaz Taherianfard, Mehdi Fazeli and Niloofar Safaei. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.