Mustafa ALTAŞ, Ahmet VAR, Can KÖSE, Kemal ÖZBİLGİN, ZEKİ ARI

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

Amaç: Gelismis ülkelerdeki diyetlerde fruktozun tüketilme sıklığı son yıllarda giderek artmaktadır. Artan fruktoz tüketimi insülin rezistansı olusturarak endotel disfonksiyonuna yol açabilir. İnsülin rezistansı, sendrom X, polikistik over sendromu, tip 2 diabet gibi birçok metabolik bozukluğun patogenezinde altta yatan etkendir. Çalısmamızın amacı, artmıs fruktoz tüketiminin, glukoz, insülin düzeylerine ve ayrıca metabolizmada kritik öneme sahip olan karaciğer dokusundaki endotel fonksiyonlarına olan etkilerini, nitrik oksit (NO) ve endothelin–1 (ET–1) ölçerek değerlendirmektir. Gereç ve yöntem: Çalısmamızda 20 erkek sıçan iki gruba ayrıldı. Çalısma grubu (grup 1, n=10) fruktozdan zenginlestirilmis izokalorik diyet ile (içeriği: %18.3 protein, %60.3 fruktoz ve %5.2 yağ), kontrol grubu ise (grup 2, n=10) purifi ye normal besin ile 2 hafta süresince beslendi. Beslenme periyodu sonrası kan ve hepatik doku örnekleri alınarak glukoz, insulin, NO ve ET–1 düzeyleri analiz edildi. Bulgular: Fruktozdan zengin beslenen sıçanlarda artmıs açlık glukozu, insülin düzeyleri ve bozulmus glukoz toleransı izlendi. Grup 1 karaciğer dokularında ise yüksek NO ve düsük ET–1 düzeyleri saptandı. Sonuç: Artmıs fruktoz tüketimi glukoz toleransını bozmakta ve insülin rezistansı olusturmaktadır. İnsülin rezistansı karaciğer dokusunda endotel disfonksiyonuna yol açabilir.

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

Objectives: Dietary high fructose consumption which is closely associated with endothelial dysfunction via insulin resistance has recently increased in developed countries. Insulin resistance has a promoter effect on many metabolic disorders such as syndrome X, polycystic ovary syndrome, 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 dysfunction 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 endothelium. 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, containing 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 hepatic tissue samples were collected and glucose, insulin, NO and ET-1 levels were analysed. Results: We found increased fasting glucose and insulin 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 deleterious effects on glucose tolerance, insulin resistance and may cause to endothelial dysfunction.

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