Endothelial dysfunction in high fructose containing diet fed rats: Increased nitric oxide and decreased endothelin-1 levels in liver tissue

Abstract

Objectives: Dietary high fructose consumption which is closely associated with endothelial dysfunction via insülin resistance has recently increased in developed countries.Insulin resistance has a promoter effect on many meta-bolic disorders such as syndrome X, polycystic ovary syn-drome, Type 2 diabetes mellitus etc. Our aim in this study is to understand the impact of increased fructose intake on metabolisms of glucose, insulin and endothelial dys-function by measuring nitric oxide (NO) and endothelin-1(ET-1) levels in hepatic tissue which is crucial in fructose metabolism. Materials and Methods: We designed an animal study to understand increased fructose intake on hepatic en-dothelium. Twenty adult male albino rats were divided into two groups; the study group (group 1, n=10) received isocaloric fructose enriched diet (fructose-fed rats, con-taining 18.3% protein, 60.3% fructose and 5.2% fat) while the control group received purifi ed regular chow (group 2,n=10) for 2 weeks. After feeding period, blood and hepatictissue samples were collected and glucose, insulin, NO and ET-1 levels were analysed. Results: We found increased fasting glucose and insülin levels and impaired glucose tolerance in fructose fed rats. Higher NO and lower ET–1 levels were also detected in hepatic tissue samples of the group 1. Conclusion: Increased fructose consumption has delete- rious effects on glucose tolerance, insulin resistance and may cause to endothelial dysfunction. Key words: Fructose consumption, endothelial dysfunc-tion, nitric oxide, endothelin-1, liver.

Keywords

• Fructose consumption, endothelial dysfunc-tion, nitric oxide, endothelin-1, liver.

Yüksek fruktoz içeren diyetle beslenen ratlarda endotel disfonksiyonu: Karaciğerdokusunda artmıs nitrik oksit ve azalmıs endotelin-1 düzeyleri

Abstract

Amaç: Gelismis ulkelerdeki diyetlerde fruktozun tüketilme sıklığı son yıllarda giderek artmaktadır. Artan fruktoz tuke-timi insulin rezistansı olusturarak endotel disfonksiyonuna yol acabilir. İnsulin rezistansı, sendrom X, polikistik over sendromu, tip 2 diabet gibi bircok metabolik bozukluğun patogenezinde altta yatan etkendir. Calısmamızın amacı, artmıs fruktoz tuketiminin, glukoz, insulin duzeylerine ve ayrıca metabolizmada kritik oneme sahip olan karaciğer dokusundaki endotel fonksiyonlarına olan etkilerini, nitrik oksit (NO) ve endothelin–1 (ET–1) olcerek değerlendir-mektir. Gereç ve yöntem: Calısmamızda 20 erkek sıcan iki gruba ayrıldı. Calısma grubu (grup 1, n=10) fruktozdan zenginlestirilmis izokalorik diyet ile (iceriği: %18.3 protein, %60.3 fruktoz ve %5.2 yağ), kontrol grubu ise (grup 2, n=10) purifi ye normal besin ile 2 hafta suresince beslendi. Beslenme periyodu sonrası kan ve hepatik doku ornekle-ri alınarak glukoz, insulin, NO ve ET–1 duzeyleri analiz edildi. Bulgular: Fruktozdan zengin beslenen sıcanlarda artmış aclık glukozu, insulin duzeyleri ve bozulmus glukoz tole-ransı izlendi. Grup 1 karaciğer dokularında ise yuksek NO ve dusuk ET–1 duzeyleri saptandı. Sonuç: Artmıs fruktoz tuketimi glukoz toleransını boz-makta ve insulin rezistansı olusturmaktadır. İnsulin rezis-tansı karaciğer dokusunda endotel disfonksiyonuna yol acabilir.

Keywords

• Fruktoz tuketimi, endotel disfonksiyo-nu, nitrik oksit, endotelin–1, karaciğer.

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