The effect of phosphorus manipulation on the progression of non-alcoholic fatty liver disease in rats maintained on a high fructose diet -

Abstract

Non Alcoholic Fatty Liver Disease (NAFLD) is an emerging disease associated with metabolic dysfunction. It is characterized by the excessive accumulation of lipids in the form of triglycerides in hepatic tissues of patients who do not consume large amounts of alcohol. High fructose feeding has been used to develop NAFLD, which is reported to be associated with Fructose intake. Fructose is known to sequester phosphorus and making it unavailable for the production of ATP. At this point, attention is raised to the role of phosphorus in fructose-induced fatty liver disease and to what extent the manipulation of phosphorus can affect this disease. The aim of the following study is to investigate the effect of different phosphorus-content diets on rats having high fructose intake, to test for the role of phosphorus in the development of NAFLD Following adaptation, forty three male Sprague-Dawley rats were randomly divided into one control group (30percent sucrose and 30percentstarch) and four high fructose (60percent) groups with different levels of phosphorus: 0.15percent-0.3percent-0.6percent and 0.9percent. After 10 weeks rats were sacrificed by decapitation. Food intake and body weight was measured twice per week. Liver biopsy along with plasma analysis was performed. Steatosis was assessed by histologic examination of Hematoxylin and Eosin (HandE) stained liver tissue sections, whereby macrovesicluar steatosis was graded from 0 to 3 and microvesicular steatosis from 0 to 1. Histologic quantitation of steatosis was also performed by image analysis of liver sections stained with Oil Red O. The results showed that high fructose diet reduced body weight by 9percent compared to control group. High fructose diet did result in any macrovesicular steatosis. Microvesicular steatosis was more frequent in the high phosphorus groups. A Zone 3 distribution was the most common pattern in HF-0.15percentP and HF-0.3percentP groups while zone 1 distribution of steatosis dominated the HF-0.6percentP and HF-0.9percentP groups. In this study, maintaining rats on high fructose diet did not induce sign