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16 research original article DISCUSSION Figure 3. Effect of DLBS3233 (9 mg/kg body weight) on the HOMA level of Wistar strain rats. In this study, we demonstrate the effect of DLBS3233 in insulin resistant animal model. The animals were treated to be insulin resistant by administration of high amount of fructose and glucose, which may lead to uncontrolled insulin action. Previous studies provide direct evidence that the insulin resistance occurs due to changes in hepatic carbohydrate metabolism, leading to increased hepatic glucose efflux under basal conditions, and to a loss of the ability of insulin to suppress hepatic glucose efflux. These changes are most likely due to an effect of fructose at several control steps in the regulation of hepatic glycogenesis, glycogenolysis and/or gluconeogenesis. 8 Insulin resistant condition induced by treatment of sugar showed that the levels of random glucose, postprandial glucose, and fasting glucose as well as insulin increased significantly when compared to control group treated with only normal saline. However, administration of DLBS3233 to the insulin resistant rats for two weeks could reverse the levels of glucose and insulin into the levels similar to those of normal condition (Table 1 and Fig. 1). Insulin resistance may occur through different mechanisms, including defects in insulin binding and signal transduction, or defects at the level of effector molecules such as glucose transporters and enzymes involved in carbohydrate metabolism. 9 DLBS3233 demonstrated its activity in controlling blood glucose by mediating the upregulation of PPARγ and GLUT4 MEDICINUS 24(1), January 2011 expression. Activation of PPARγ induces adipocyte differentiation and lipid accumulation by adipocytes through modulating numerous genes regulating adipogenesis, lipid uptake and lipid metabolism. Result of that study also indicated that DLBS3233 is a glucose transport-stimulant as it upregulates GLUT4 expression significantly. 10 Fructose feeding may result in hypertriglyceridemia, resistance to insulin-stimulated glucose uptake, and impaired endothelium-dependent vasodilation, but not in an elevation of arterial pressure. In the fructose-fed rat, hypertriglyceridemia has been attributed to impaired triglyceride removal due to insulin resistance. 11 In addition, hypertiglyceridemia also has a strong correlation with increased LDLcholesterol and decreased HDL-cholesterol. 3 Results of this study also showed that levels of other biological parameters including total cholesterol, LDL, and triglycerides were increased in insulin-resistant model while the level of HDL for the insulin resistant group decreased. However, the levels of those biological parameters were back to normal when DLBS3233 was administered in the treated rats. This finding suggests that DLBS3233 posses the ability to control the triglyceride and cholesterol level including LDL and HDL level. Furthermore, indirect method for assesment of insulin resistance was also perfomed by determining HOMA level. It is usually perfomed for early identification of insulin resistant individuals as it is important for the management strategies of diabetes mellitus. HOMA (homeostasis model assesment) is a
commonly used method to assess insulin resistance and ß-cell function and requires only fasting glucose and insulin levels. 12 It is believed that HOMA index possesses high sensitivity and specificity for measuring insulin resistance. 13 In this study, the HOMA index was significantly reduced to normal after DLBS3233 administration suggesting that DLBS3233 has a strong activity to control insulin resistant condition (Fig. 2 and 3). Taken together, this study indicates that DLBS3233 has the activity to control blood sugar, in- References 1. Laakso M. Hyperglycemia and cardiovascular disease in type 2 diabetes. Diabetes 1999; 48(5):937-42 2. Bressler P, Bailey SR, Matsuda M, DeFronzo RA. Insulin resistance and coronary heart disease. Diabetologia 1996; 39:1345-50 3. Taghibiglou C, Carpentier A, Iderstine SCV, Chen B, Rudy D, Aiton A, et al. Mechanisms of hepatic very low density lipoprotein overproduction in insulin resistance. J Biol Chem 2000; 275(12):8416-25 4. Liu F, Kim J-K, Li Y, Liu X, Li J, Chen X. An extract of Lagerstroemia speciosa L. has insulin like glucose uptake stimulatory and adipocytes differentiation-inhibitory activities in 3T3-L1 cells. J Nutr 2001; 131:2242-7 5. Liu X, Kim J-K, Li Y, Li J, Liu F, Chen X. Tannic acid stimulates glucose transport and inhibits adipocyte differentiation in 3T3-L1 cells. J Nutr 2004; 135:165-71 6. Sheng X, Zhang Y, Gong Z, Huang C, Zang YQ. Improved insulin resistance and lipid metabolism by cinnamon extract through activation of peroxisome proliferator-activated receptors. PPAR Res 2008; 2008:581348 7. Pickavance LC, Tadayyon M, Widdowson PS, Buckingham RE, Wilding JPH. Therapeutic index for rosiglitazone in dietery obese rats: separation of efficacy and haemodilution. Br J Pharmacol 1999; 128:1570-6 sulin and other lipoproteins including High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL), triglycerides, and total cholesterol level. Accordingly, DLBS3233 is suggested to be a potential agent for treatment of diabetes and minimizing the risk of that diabetic complication including atherosclerosis. ACKNOWLDEgMENTS original article research We thank Audrey Clarissa and Venni Carolina for critical review on this manuscript. 8. Tobey TA, Mondon CE, Zavaroni I and Reaven GM. Mechanism of insulin resistance in fructose-fed rats. Metabolism 1982; 31(6):608- 12 9. Catena C, Giacchetti G, Novello M, Colussi G, Cavarape A, Sechi LA. Cellular mechanisms of insulin resistance in rats with fructoseinduced hypertension. Am J Hypertens 2003; 16(11):973-8 10. Tandrasasmita OM, Wulan DDR, Nailufar F, Sinambela J, Tjandrawinata RR. In press. DLBS3233 increases glucose uptake by mediating upregulation of PPARγ and GLUT4 expression. J Biomed Biotech. 11. Kotchen TA, Reddy S, Zhang HY. Increasing insulin sensitivity lowers blood pressure in the fructose-fed rat. Am J Hypertens 1997; 10:1020–6 12. Chang AM, Smith MJ, Bloem CJ, Galecki AT, Halter JB, Supiano MA. Limitation of the homeostasis model assessment to predict insulin resistance and beta-cell dysfunction in older people. J Clin Endocrinol Metab 2006; 91(2):629-34 13. Keskin M, Kurtoglu S, Kendirci M, Atabek ME, Yazici C. Homeostasis model assessment is more reliable than the fasting glucose/insulin ratio and quantitative insulin sensitivity check index for assessing insulin resistance among obese children and adolescents. Pediatrics 2005; 115(4):500-3 MEDICINUS 24(1), January 2011 17
Page 3 and 4: Chief Editor Dr. Raymond R. Tjandra
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Page 15 and 16: Effect of DLBS3233, an Insulin Sens
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