Niacin Ameliorates Lipid Disturbances due to Glucocorticoid Administration in Rats

Authors

1 Division of Physiology, Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran

2 Division of Pharmacology and Toxicology, Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran

Abstract

Objective(s)
This study was conducted to evaluate the effects of niacin on glucocorticoid-induced dyslipidemia and fatty liver in rats.
Materials and Methods
Twenty four adult male rats were divided randomly into four equal groups: 1- normal saline (control), 2- dexamathasone 0.125 mg/kg/day, i.m., 3- dexamathasone + niacin 200 mg/kg/day, oral gavages, 4- niacin. After 2 weeks, serum total cholesterol, triglycerides, HDL-c, LDL-c and VLDL-c concentrations were assayed and liver sections examined for fatty liver changes. Data were analyzed by ANOVA method and         P< 0.05 was considered significant.
Results
Dexamethasone increased all lipid parameters as compared to control (P< 0.05). Lipid parameters in group 3, were lower than group 2 (P< 0.05) except for HDL-c which remained statistically the same. Moderate fatty liver changes were observed in one third of rats in dexamethasone group. Rats in groups 1, 3 and 4 had no sign of fatty changes.
Conclusion
Niacin positively affects glucocorticoid-induced dyslipidemia and fatty liver changes in rats.

Keywords


1. Schimmer BP, Parker KL. Adrenocorticotropic hormone; adrenocortical steroids and their synthetic analogs; inhibitors of the synthesis and actions of adrenocortical hormones. In: Goodman and Gilman's the Pharmacological Basis of Therapeutics. 10th ed. United states of America: McGraw-Hill; 2001. p.1649-1677.

2. Plumb DC. Plumb's Veterinary Drug Handbook. 6th ed. Iowa: Blackwell Publishing; 2008.

3. Jefferys DB, Lessof MH, Mattock MB. Corticosteroid treatment, serum lipids and coronary artery disease. Postgrad Med J 1980; 56:491-493.

4. Mitamura T. Glucocorticoid-induced elevation of serum high-density lipoprotein-cholesterol and its reversal by adrenocorticotropin in the rat. Biochim Biophys Acta  1987; 917:121-130.

5. Sholter DE, Armstrong PW. Adverse effects of corticosteroids on the cardiovascular system. Can J Cardiol  2000; 16:505-511.

6. Arnaldi G, Scandali VM, Trementino L, Cardinaletti M, Appolloni G, Boscaro M. Pathophysiology of dyslipidemia in Cushing's syndrome. Neuroendocrinology 2010; 92:86-90.

7. Letteron P, Brahimi-Bourouina N, Robin MA, Moreau A, Feldmann G, Pessayre D. Glucocorticoids inhibit mitochondrial matrix acyl-CoA dehydrogenases and fatty acid beta-oxidation. Am J Physiol  1997; 272:1141-1150.

8. Westphal S, Borucki K, Taneva E, Makarova R, Luley C. Extended-release niacin raises adiponectin and leptin. Atherosclerosis 2007; 193:361-365.

9. Bagdade JD,Yee E, Albers J, Pykalisto OJ. Glucocorticoids and triglyceride transport: effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. Metabolism  1976; 25:533-542.

10. Barboriak JJ, Meade RC. Nicotinic acid and alcohol-induced lipemia. Atherosclerosis 1971; 13:199-203.

11. Vegiopoulos A, Herzig S. Glucocorticoids, metabolism and metabolic diseases. Mol Cell Endocrinol 2007; 275:43-61.

12. Jin FY, Kamanna VS, Kashyap ML. Niacin decreases removal of high-density lipoprotein apolipoprotein A-I but not cholesterol ester by Hep G2 cells. Implication for reverse cholesterol transport. Arterioscler Thomb Vasc Biol 1997; 17:2020 –2028.

13. Ganji SH, Tavintharan S, Zhu D, Xing Y, Kamanna VS, Kashyap ML. Niacin noncompetitively inhibits DGAT2 but not DGAT1 activity in HepG2 cells. J Lipid Res  2004; 45:1835–1845.

14. Shepherd J, Betteridge J, Van Gaal L. Nicotinic acid in the management of dyslipidaemia associated with diabetes and metabolic syndrome: a position paper developed by a European Consensus Panel. Curr Med Res Opin 2005; 21:665-682.

15. Cole TG, Wilcox HG, Heimberg M. Effects of adrenalectomy and dexamethasone on hepatic lipid metabolism. J Lipid Res 1982; 23:81-91.