The effects of resveratrol on biochemical changes in fructose-induced insulin resistance

Yıl 2011, , 339 - 346, 01.12.2011

Nevin İlhan Dilara Kaman Necip İlhan

https://doi.org/10.5799/ahinjs.01.2011.04.0069

Cited By: 1

Öz

Objectives: The present study aimed to evaluate the influence of resveratrol (RSV) administration on biochemical parameters, free fatty acids (FFAs), cytokines and chemokines of rats administered high dose of fructose. Materials and methods: Rats fed with fructoses that form an experimental animal model of the metabolic syndrome. Adult Wistar rats were divided into three groups of 5 rats each. In Groups 1, animals received starch-based control diet, while groups 2 and 3 rats were fed a high-fructose diet. Groups 3 animals additionally received RSV (10 mg/kg) daily for 20 days after 40 days fed with fructose. The levels of glucose, insulin, cholesterol and triglyceride were measured by using an enzymatic assay on an Auto analyzer. Serum levels of FFAs were measured by Gas Chromatography and cytokines such as MCP-1, IL-10, RANTES and eotaxin levels were measured by ELISA. Results: Fructose-fed rats exhibited increased levels of glucose, insulin, HOMA-IR index and FFAs. Eotaxin, RANTES and TNF-α levels were also increased in fructose fed rats. RSV administration improved biochemical parameters as well as FFAs in an experimental animal model of the metabolic syndrome. Conclusion: The benefits of RSV observed in this model suggest that therapeutic use of RSV may be thought in metabolic syndrome. J Clin Exp Invest 2011; 2 (4): 339-346

Anahtar Kelimeler

fructose diet, resveratrol, free fatty acids, cytokines, chemokines

The effects of resveratrol on biochemical changes in fructose-induced insulin resistance

Öz

Amaç: Bu çalışmada, fruktozun yüksek dozu verilen sıçanlarda resveratrolun (RSV), serbest yağ asitleri (SYAleri), sitokinler ve kemokinler gibi biyokimyasal parametreler üzerine etkisinin değerlendirilmesi amaçlandı. Gereç ve yöntem: Metabolik sendromun bu deneysel hayvan modelinde sıçanlar fruktozla beslendi. Erişkin Wistar cinsi sıçanlar her birinde 5 sıçan olacak şekilde üç gruba ayrıldı. Grup 1, nişasta bazlı kontrol diyeti aldı. Grup 2 ve 3 sıçanlar yüksek fruktoz diyeti ile beslendi. 40 gün fruktoz ile beslenen Grup 3 sıçanlara daha sonra 20 gün boyunca günlük resveratrol (10 mg / kg) uygulaması yapıldı. Otoanalizörde enzimatik analiz yöntemleri kullanılarak glukoz, insülin, kolesterol ve trigliserid düzeyleri ölçüldü. SYA\'leri Gaz Kromatografisi ile MCP-1, IL-10 RANTES ve eotaksin gibi sitokinlerin serum düzeyleri ise ELISA yöntemi ile ölçüldü. Fruktoz ile beslenen sıçanlarda artmış glukoz, insülin, HOMA-IR indeksi ve FFAs seviyeleri tespit edildi. Bulgular: Eotaksin, RANTES ve TNF-α düzeyleri de fruktozla beslenen sıçanlarda artmıştı. Resveratrol uygulaması, metabolik sendromun bu deneysel hayvan modelinde biyokimyasal parametrelerin yanı sıra SYA\'lerini de olumlu etkiledi. Sonuç: Bu modelde gözlenen yararlı etkileri nedeniyle metabolik sendromda RSV\'un tedavide kullanımı düşünülebilir.

Anahtar Kelimeler

Fruktozlu diyet, resveratrol, serbest yağ asitleri, sitokinler, kemokinler

Kaynakça

• Zavaroni I, Sander S, Scott S, Reaven GM. Effect of fructose feeding on insulin secretion and insulin action in the rat. Metabolism 1980; 29 (10): 970-3.
• Reaven GM. Syndrome X: 6 years later. J Intern Med 1994; 736: 13-22.
• Basciano H, Federico L, Adeli K. Fructose, insulin re- sistance, and metabolic dyslipidemia. Nutr Metab 2005; 2 (1): 5-8.
• Rivera L, Morón R, Zarzuelo A, Galisteo M. Long-term resveratrol administration reduces metabolic distur- bances and lowers blood pressure in obese Zucker rats. Biochem Pharmacol 2009; 77 (6): 1053-63.
• Dandona P, Aljada A, Bandyopadhyay A. Inflammation: the link between insulin resistance, obesity and diabe- tes. Trends Immunol 2004; 25 (1): 4-7.
• Mazur A, Maier JAM, Rock E, Gueux E, Nowacki W, Rayssiguier Y. Magnesium and the inflammatory re- sponse: potential physiopathological implications. Arch Biochem Biophys 2007; 458(1):48-56.
• Sjöholm A, Nyström T. Endothelial inflammation in insu- lin resistance. Lancet 2005; 365(9459):610-2.
• Sjöholm A, Nyström T. Inflammation and the etiology of type 2 diabetes. Diabetes Metab Res Rev 2006; 22(1):4-10.
• Nielsen S, Guo Z, Johnson CM, Hensrud DD, Jensen MD. Splanchnic lipolysis in human obesity. J Clin In- vest 2004; 113(11):1582-8.
• Bhat KPL, Kosmeder JW 2nd, Pezzuto JM. Biologi- cal effects of resveratrol. Antioxid Redox Signal 2001; 3(6):1041-64
• Robb EL, Page MM, Wiens BE, Stuart JA. Molecu- lar mechanisms of oxidative stress resistance in- duced by resveratrol: Specific and progressive in- duction of MnSOD. Biochem Biophys Res Commun 2008;367(2):406-12.
• Szkudelska K, Szkudelski T. Resveratrol, obesity and diabetes. Eur J Pharmacol 2010;635(1-3):1-8.
• Bertelli AA, Das DK. Grapes, wines, resveratrol and heart health. J Cardiovasc Pharmacol 2009;54(6):468- 76.
• Bishayee A. Cancer prevention and treatment with resveratrol: from rodent studies to clinical trials. Can- cer Prev Res 2009;2(5):409-18.
• Ashcroft F, Rorsman P. Type 2 diabetes mellitus: not quite exciting enough? Hum Mol Genet 2004;13 (1):R21-31
• Tsai SH, Lin-Shiau SY, Lin JK. Suppression of nitric oxide synthase and the down-regulation of the activa- tion of NFkappa B in macrophages by resveratrol. Br J Pharmacol 1999;126(3):673-80.
• Sánchez-Lozada LG, Tapia E, Jiménez A, Bautista P, et al. Fructose-induced metabolic syndrome is asso- ciated with glomerular hypertension and renal micro- vascular damage in rats. Am J Physiol Renal Physiol. 2007;292(1):F423-9.
• Hascalik S, Celik O, Turkoz Y, et al. Resveratrol, a red wine constituent polyphenol, protects from ischemia- reperfusion damage of the ovaries. Gynecol Obstet Invest 2004; 2004;57(4):218-23.
• Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assess- ment: insulin resistance and beta cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28(7):412-9.
• Meng Y, Wang G, Yang N, et al. Two-step synthesis of fatty acid ethyl ester from soybean oil catalyzed by Yarrowia lipolytica lipase. Biotechnol Biofuels 2011;4(1):6-9.
• Rutledge AC, Adeli K. Fructose and the Metabolic Syndrome: Pathophysiology and Molecular Mecha- nisms. Nutr Rev 2007;65(6 Pt 2):S13-23.
• Crespin SR, Greenough WB III, Steinberg D. Stim- ulation of insulin secretion by long-chain free fatty acids. A direct pancreatic effect. J Clin Invest 1973; 52(8):1979-84.
• Peiris AN, Mueller RA, Smith GA, Struve MF, Kisse- bah AH. Splanchnic insulin metabolism in obesity. Influence of body fat distribution. J Clin Invest 1986; 78(6):1648-57.
• Liu RH, Mizuta M, Kurose T, Matsukura S. Early events involved in the development of insulin resistance in Zucker fatty rat. Int J Obes Relat Metab Disord 2002; 26(3):318-26.
• Fernández-Veledo S, Nieto-Vazquez I, Vila-Bedmar R, et al. Molecular mechanisms involved in obesity- associated insulin resistance: therapeutical approach. Arch Physiol Biochem 2009; 115(4):227-39.
• Hotamisligil GS, Budavari A, Murray D, Spiegelman BM. Reduced tyrosine kinase activity of the insulin re- ceptor in obesity-diabetes: central role of tumor necro- sis factor-alpha. J Clin Invest 1994; 94(4):1543-9.
• Hopkins PN, Hunt SC, Wu LL, Williams GH, Williams RR. Hypertension, dyslipidemia and insulin resis- tance: links in a chain or spokes on a wheel? Curr Opin Lipidol 1996; 7(4):241-53.
• Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM. IRS-1-mediated inhibition of in- sulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. Science 1996; 271(5249):665-8.
• Hsueh WA, Law RE. Insulin signaling in the arterial wall. Am J Cardiol 1999;84(1A):21J-24J.
• van Exel E, Gussekloo J, de Craen AJ, Frölich M, Bootsma-Van Der Wiel A, Westendorp RG. Low Pro- duction Capacity of Interleukin-10 Associates with the Metabolic Syndrome and Type 2 Diabetes: the Leiden 85-Plus Study. Diabetes 2002; 51(4):1088-92.
• Duncan BB, Schmidt MI. Chronic activation of the in- nate immune system may underlie the metabolic syn- drome. Sao Paulo Med J 2001; 119(3):122-7.
• Forsythe CE, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM, Kraemer WJ, Feinman RD, Volek JS. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and mark- ers of inflammation. Lipids 2008; 43(1):65-77.
• Veillard NR, Kwak B, Pelli G, et al. Antagonism of RANTES receptors reduces atherosclerotic plaque formation in mice. Circ Res 2004; 94(2):253-61.
• Herder C, Haastert B, Müller-Scholze S, et al. Asso- ciation of Systemic Chemokine Concentrations with Impaired Glucose Tolerance and Type 2 Diabetes: Results from the Cooperative Health Research in the Region of Augsburg Survey S4 (KORA S4). Diabetes 2005 Dec;54 Suppl 2:S11-7.
• Vasudevan AR, Wu H, Xydakis AM, et al. Eotaxin and obesity. J Clin Endocrinol Metab 2006;91(1):256-61.
• Dell’Agli M, Busciala A, Bosisio E. Vascular effects of wine polyphenols. Cardiovasc Res 2004; 63(4):593- 602.
• Milne JC, Lambert PD, Schenk S, et al. Small molecule activators of SIRT1 as therapeutics for the treatment of type 2 diabetes. Nature 2007; 450(7170):712-6.
• Olholm J, Paulsen SK, Cullberg KB, Richelsen B, Pedersen SB. Anti-inflammatory effect of resveratrol on adipokine expression and secretion in human adi- pose tissue explants. Int J Obesity 2010;34(10):1546- 53.
• Marier JF, Chen K, Prince P, Scott G, del Castillo JR, Vachon P. Production of ex vivo lipopolysaccharide- induced tumor necrosis factor-α, interleukin-1β, and inter-leukin-6 is suppressed by trans resveratrol in a concentration-dependent manner. Can J Vet Res 2005; 69(2):151-4.
• Yki-Järvinen H. Liver fat in the pathogenesis of in- sulin resistance and type 2 diabetes. Dig Dis 2010;28(1):203-9.