Objective(s) This study was conducted to evaluate the effects of niacin on glucocorticoid-induced dyslipidemia and fatty liver in rats. and osteoporosis (2). Moreover GCs can elevate plasma lipids in humans (3) and induce dyslipidemia in laboratory animals (4); in a way that these agents have been identified as a second reason behind dyslipidemia. The fact that pharmacologic doses of GCs can affect plasma lipid levels has been known for decades. It has been extensively shown that GC administration is associated with serum lipid disturbances including elevations in total cholesterol triglycerides LDL-c and HDL-c in humans (5) as well as laboratory animals (4). Moreover dyslipidemia may be present in humans with Cushing’s syndrome (6). On the other hand GCs are known to contribute to fatty liver production (7) and a high prevalence (up to 20%) of fatty liver has been reported in people afflicted with Cushing’s syndrome (6). Since its initial elucidation more than 50 years ago in a land mark study by Altshul niacin (nicotinic acid or vitamin B3) administration has shown beneficial effects on traditional lipoprotein fractions. This agent has recently attracted renewed interest; first because it is currently IMPG1 antibody the most potent drug increasing HDL-c and secondly because it has been found to induce regression of atherosclerosis (8). However effects of niacin on GC-induced lipid disturbances CEP-18770 have not been clarified. Regarding the particular feature of GC-induced dyslipidemia (high HDL-c CEP-18770 levels) The present study was conducted to evaluate effects of niacin on dyslipidemia and fatty changes of liver due to dexamethasone a potent GC receptor agonist with insignificant mineralocorticoid receptor activity in rats as a frequently used animal model for dyslipidemic conditions. Materials and Methods 1976 and Barboriak and Meade 1971 respectively (9 10 Animals had free access to tap water and standard rat chow diet prepared by Razi Vaccine and Serum Research Institute . All animals were weighed daily during the experiment. All Procedures used were in accordance with Institutional Ethical Guidelines of School of Veterinary Medicine Shiraz University for care and use of laboratory animals in experiments. test (SPSS 11.5 software CEP-18770 for windows). Differences were considered significant at 1976 observed significant increases in triglycerides and VLDL triglyceride associated with no change in cholesterol and a CEP-18770 genuine decrease in both triglyceride and cholesterol in LDL in rats treated with dexamethasone for 14 days (9). With this scholarly research particular actions were under taken up to maintain positive caloric stability. In the analysis performed by Cole 1982 dexamethasone administration for seven days in rats improved the focus of plasma free of charge essential fatty acids and triglycerides along with VLDL proteins triglyceride phospholipid and free of charge cholesterol. Zero noticeable adjustments had been seen in the focus or structure of plasma LDL lipids. The focus of plasma HDL proteins and lipid tended to improve (15). In today’s research dexamethasone administration induced a clear dyslipidemia that was proven by elevations in serum degrees of total cholesterol triglycerides LDL-c HDL-c and VLDL-c. The incomplete discrepancies CEP-18770 seen in serum lipid guidelines among different research may be because of different dosages treatment intervals agents and the complete condition from the tests. Treatment of rats with GCs offers led to build up of lipids in the liver organ (15). In today’s research dexamethasone induced moderate examples of fatty liver organ in a single third of dexamethasone treated rats that was not seen in dexamethasone+niacin treated rats. Concerning the lipid profile niacin considerably lowered total cholesterol triglycerides LDL-c and VLDL-c levels as compared to dexamethasone treated rats. The only serum lipid parameter of dexamethasone+niacin treated rats that reduced to the control level was total cholesterol. It seems that although niacin can extenuate dyslipidemia due to GC administration it cannot completely reverse it to the normal values. Another interesting finding was the fact that the level of HDL-c in rats treated with dexamethasone+niacin remained higher than control group and statistically the same as rats treated with dexamethasone. This may be due to the intrinsic property of.