Krill veya Balık Yağı Verilen Sıçanlarda Obeziteye ve Lipit Gen Ekspresyonuna İlişkin Bazı Parametrelerin İncelenmesi
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Date
2018-02-22Author
Aydın Çil, Mevra
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The aim of this project was to determine the effect of n-3 LCPUFA supplementation the prevention and treatment of obesity and obesity related diseases, and to compare the effectiveness of different n-3 LCPUFA sources via biochemical and genetic mechanisms in rats. Thirty three male Wistar rats were classified into four study groups and fed for eight weeks with a standart diet, a High Fat Diet (HFD), a a High Fat Diet+%2.5 fish oil (FO-HFD) or a High Fat Diet+%2.5 krill oil (KO-HFD). At the end of eight weeks, rats were sacrified, and blood and liver tissue samples were taken. The amount of pellet food consumed, weight gain, serum glucose, insulin, ghrelin and leptin concentrations, lipid profile, liver fatty acid composition and fatty acid desaturase 1 and 2 (FADS1 and FADS2) mRNA gene expression levels of rats were measured. The amount of pellet feed consumed by each group was significantly differed with a minimum consumption in FO-HFD group (p<0.05). Weight gain in each study group was significantly higher than control group (p<0.05); however, n-3 LCPUFA did not change weight gain of rats significantly (p>0.05). Serum glucose, total cholesterol (TC), triglycerides (TG) and low density lipoprotein cholesterol (LDL-C) were higher in all HFD groups compared to control group (p<0.05). On lipid profile n-3 LCPUFA supplementation provided favourable effects; however, did not change glucose tolerance (p>0.05). Serum TC level of KO-HFD group was significantly lower than both HFD and BO-HFD groups (p<0.05); also, serum TG level of the KO-HFD group was significantly lower than only HFD group (p<0.05). There was no difference between serum ghrelin levels of groups (p>0.05), but serum leptin levels was higher in HFD vs control (p<0.05). n-3 LCPUFA supplementation did not change the liver n-6/n-63 fatty acid ratio (p>0.05). Liver n-3 fatty acid desaturation activity was higher, and liver total lipid content was lower in KO-HFD compared to BO-HFD (p>0.05). FADS1 gene expression was higher in the HFD (p<0.05); FADS1 gene expression decreased in BO-HFD and KO-HFD groups (p<0.05). When compared to other groups FADS2 gene expression level was higher in the BO-HFD group (p<0.05); krill oil did not affect the FADS2 gene expression level (p>0.05). As a result, it was showed that n-3 LCPUFA supplementation from different resources regulate lipid metabolism and expression of desaturase genes differently in rats. In light of the results of this preclinical study, randomized controlled trials are needed to determine the efficacy and different types of n-3 LCPUFA in the treatment and prevention of diseases associated with obesity and obesity in human metabolism.