果糖攝取已伴隨代謝症候群盛行率有攀升的趨勢，而在流行病學上代謝症候群與腎臟損傷的發展極具相關性。本研究假設果糖不同的代謝路徑，在小鼠也許會導致不同的生理和腎臟組織形態反應的變化程度。而研究目的主要是探討20%果糖飲水誘發慢性腎損傷之動物模式，運用蘇木紫-伊紅染色方法觀察小鼠腎臟組織切片是否造成慢性損傷，並探討果糖對於小鼠腎臟組織病理形態影響及定量分析。結果顯示飲食中添加20%果糖介入在組織病理學形態方面發現，果糖會造成腎臟中鮑氏囊數目顯著減（P<0.01），且腎血管和鮑氏囊基底膜有增厚的趨勢，而鮑氏囊也出現明顯紅血球堆積的情形(P<0.01)。由此可知，根據本研究發現餵食20%果糖可能會誘發小鼠慢性腎損傷的發生，而果糖誘發腎臟功能紊亂與代謝症候群有關。因此，飲食中果糖的消耗與慢性腎損傷的發展將更值得被關注Fructose intake has been associated with increased prevalence of metabolic syndrome a trend, and in the epidemiology of metabolic syndrome and the development of renal injury in very relevant.It is hypothesized that different metabolic pathways of fructose,in mice may lead to different physiological and morphological response to changes in kidney level. The purpose of this study was to explore the drinking water of 20% fructose-induced animal model of chronic renal damage.using Hematoxylin & eosin staining of renal biopsy is caused by chronic injury, and to explore the fructose for the Morphology of renal pathology in mice and quantitative analysis. The results showed that diet containing 20% fructose involved in histopathological patterns found that fructose can
cause kidney significantly reduce the number of Martin's capsule (P <0.01), and renal vascular and Martin's capsule basement membrane thickening trend Powell also showed a visible capsule case of accumulation of red blood cells (P <0.01). It can be seen，this study found that 20% of fructose fed mice may induce the occurrence of chronic renal injury, while fructose-induced kidney disorders and metabolic syndrome. Therefore, the consumption of fructose diet and chronic renal injury in development will be more worthy of attention.
