Farelerde Diyet Yağ Asitleri ve Fruktozun Bazı İnflamatuar Medyatörler ve Yağ Asit Biyosentezi Üzerine Etkileri
Özet
Tamer, F., The Effects of Dietary Fatty Acids and Fructose on Some Inflammatory Mediators and Fatty Acid Biosynthesis in Mice, Hacettepe University Institute of Health Sciences Nutrition and Dietetics Program, Doctor of Philosophy Thesis, Ankara, 2017. Currently, consumption of high quantities of fructose and saturated fatty acids via processed food is recognized as a central factor in the development of chronic disease. The aim of this study was to investigate the effects of dietary high saturated fatty acid or fructose on lipogenesis, insulin resistance and inflammation. The study was performed on the C57Bl/6 type male mice (n=40, 8 weeks old) with ad libitum access to chow diet and three different type of diets enriched with two different fatty acids (refined olive oil, coconut oil) and carbohydrate (fructose) types for 15-weeks. At the end of the dietary period, the animals were sacrificed; then organ and tissues isolated immediately. As a result, it was found that mean feed intake of fructose fed group was higher (p<0,05). Body weight change were found significantly higher in saturated fatty acid and fructose fed mice with higher energy intake than control and isocaloric high monounsaturated fatty acid fed groups (p<0,001). Plasma and liver triglyceride levels and HOMA-IR (p<0,05) values were significantly higher in high saturated fat and high fructose fed groups. Plasma free fatty acids and CRP levels were higher in fructose fed group (p<0,05). Western-blotting results for ACC-1 and phosphorylated form of ACC-1, phosphorylated IRS-1, AMPK and TLR-4 expression in liver showed that the expression levels were higher in high saturated fatty acid and high fructose fed groups. In conclusion, this study showed that to reduce the risk of chronic diseases, it is necessary to pay attention to the saturated fatty acid and fructose intake which can increase lipogenesis and inflammation accompanying with insulin resistance in the liver.