Diyetle Alınan Doymuş Yağ Asitleri veya Fruktozun Böbrek ve Kalpte Bazı Pro-İnflamatuar Sitokinler Üzerine Etkisi

Abstract

In recent years, it has been hypothesized that dietary high consumption of fructose or saturated fatty acids may play a role in the aetiology of chronic diseases by activating the pro-inflammatory mechanisms in blood and tissues. The aim of this study was to investigate the possible effects of high saturated fatty acids or high fructose containing diet on proinflammatory cytokines of plasma and storage tissues including kidney and heart. In the previous study, in which tissues were obtained, C57BL/6 type mice (n=40, 8 weeks-old), after the standardization period of 2 weeks, were divided into 4 groups and fed with standart chow (Control), high monounsaturated fatty acids (MUFA), high saturated fatty acids (SFA), high fructose (FRU) containing diets ad libitum for 15 weeks. At the end of dietary period, the mice were euthanized, then blood and tissues were isolated and the study was terminated. It was determined that feed intake in FRU group was higher than other groups (p<0,05). In parallel with energy intake of dietary manipulation groups were higher than control (p<0,001), average weight gain in these groups were higher than other groups (p<0,05). Plasma tumor necrosis factor (TNF) and interleukin (IL)-6 levels were higher in SFA or FRU groups compared to the other groups (p<0,001). Plasma monocyte chemoattractant protein-1 (MCP-1) levels were higher in the FRU group compared to the control and MUFA groups (p<0,001), but were lower in the SFA group (p<0,05). Plasma IL-10 concentrations were lower in SFA and FRU groups than control and MUFA groups. Plasma interferon-gamma (IFN-γ) and IL-12p70 levels did not differ between groups (p>0,05). According to western-blot analysis, TNF-α, IL-1β and IL-6 expression of kidney and heart tissues increased in SFA and FRU groups. Results suggests that the dietary high fructose or high saturated fatty acids might be a risk factor for chronic diseases and should therefore be limited by considering pro-inflammatory response processes in plasma blood and tissues.