Anti-Inflammatory Agent and Body Weight enced inflammatory markers. In contrast, ad libitum low- fat, high-carbohydrate intake caused weight loss and affect- ed inflammatory markers favorably. Thus, the energy content of a low-fat, high-carbohydrate diet determined changes in inflammatory markers.18 Another study reported an overall favorable effect of a low-carbohydrate diet on lipoprotein subfractions and inflammation in high-risk subjects.19 In an- other study, no significant changes were evident in either median adiponectin or IL-10 levels after body weight re- duction.20 In this study, the authors opined that the anti-in- flammatory status of obesity might require prolonged peri- ods of energy-restricted diets to revert to normal. A study in which metformin was provided for 17 weeks reported sig- nificant reduction in body weight, but not in levels of TNF-α and CRP.21 Metformin improved the plasma levels of some markers of endothelial activation and coagulation in sub- jects with impaired glucose tolerance, whereas it had no ef- fect on markers of inflammation. In a study of 316 commu- nity-dwelling, older overweight or obese sedentary men and women with osteoarthritis, diet-induced weight-loss in- tervention resulted in significantly greater reductions in CRP, IL-6, and TNF-α than treatment not intended to re- duce weight.22 In this study, CRP and IL-6 were not associ- ated with changes in body weight. The addition of cis-9, trans-11 conjugated linoleic acid also did not produce any differences between groups in body composition in a dou- ble-blind, placebo-controlled 3-month study of 25 abdomi- nally obese men.23 While a decrease in many inflammatory markers such as TNF-α, CRP-reactive protein and IL-6 were reported in another study, adiponectin levels were sig- nificantly higher after intervention.24 Many studies evaluating changes of inflammatory mark- er after different periods or regimens of weight reduction have not yielded consistent results. However, the decrease in inflammatory markers such as TNF-α, CRP, and IL-6 and increase of adiponectin level has been apparent after weight reduction.25-28 Changes in other metabolic parameters including lipid profiles, glucose level, and TNF-α were insignificant in both groups, which may be due to the small sample size. In addition, there was no adverse drug reaction in the treat- ment group for the 3-month intervention period. There are some limitations to this pilot study. The main limitation concerns the small number of subjects. This may be a crucial limitation that weakens the significance of the re- sults, but not their reality. We tried to equally allocate to each group, but there was some follow-up loss in this study for personal reasons. Furthermore, the relatively short duration of this intervention would contribute to the lack of change in inflammatory markers, as in previous studies. Another limitation is that the intervention medication we used (Dia- cerein, an anti-inflammatory agent that is a TNF-α and IL-1 inhibitor) is not an officially recognized agent in the regula- tion of inflammation in the obese. Additionally, we could not evaluate total exercise time and frequency, which are important confounding factors. Nonetheless, to our knowl- edge, this is the first randomized, placebo-controlled study that investigated the effect of inclusion of an anti-inflamma- tory agent to a traditional obesity control regimen involving medication with Sibutramine, to evaluate whether there was additional reduction of weight and of inflammatory markers. In conclusion, we did not find any additional ef- fects of Diacerein on weight loss and inflammatory vari- ables in this study. ACKNOWLEDGEMENTS This study was sponsored by the New Faculty Research Fund in Ajou University School of Medicine, Suwon, Ko- rea, 2008. REFERENCES 1. Korean Ministry of Health and Welfare. Report on National Health and Nutrition Survey 2005. Seoul: Korean Ministry of Health and Welfare; 2006. 2. Jee SH, Sull JW, Park J, Lee SY, Ohrr H, Guallar E, et al. Body mass index and mortality in Korean men and women. N Engl J Med 2006;355:779-87. 3. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. El- evated C-reactive protein levels in overweight and obese adults. JAMA 1999;282:2131-5. 4. Cook DG, Mendall MA, Whincup PH, Carey IM, Ballam L, Mor- ris JE, et al. C-reactive protein concentration in children: relation- ship to adiposity and other cardiovascular risk factors. Atheroscle- rosis 2000;149:139-50. 5. Wisse BE. The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity. J Am Soc Nephrol 2004;15:2792-800. 6. Bastard JP, Maachi M, Lagathu C, Kim MJ, Caron M, Vidal H, et al. Recent advances in the relationship between obesity, inflamma- tion, and insulin resistance. Eur Cytokine Netw 2006;17:4-12. 7. Ramalho R, Guimarães C. [The role of adipose tissue and macro- phages in chronic inflammation associated with obesity]. Acta Med Port 2008;21:489-96. 8. Ford ES. The metabolic syndrome and mortality from cardiovas- cular disease and all-causes: findings from the National Health Yonsei Med J http://www.eymj.org Volume 52 Number 2 March 2011 247