The role of phosphorus in the development and progression of high fat diet induced NAFLD in rats -

Abstract

The term non-alcoholic fatty liver disease (NAFLD) refers to the range of diseases characterized by fatty infiltration of the liver ranging from benign steatosis, to the more severe steatohepatitis, or cirrhosis. Interest is raised on the relationship between dietary phosphorus and NAFLD since a recent study showed that dietary Pi restriction plays an important role in the development of fatty liver disease and hyperlipidemia induced by a high-cholesterol diet through regulation of lipid metabolism–related gene expression in the liver. Likewise, hypophosphatemia has been reported in studies of large numbers of individuals with metabolic syndrome. Therefore, it was hypothesized that phosphorus seems to embody the missing link between the metabolic derangements that occur in metabolic syndrome and NAFLD. The aim of this study is to investigate the role of dietary phosphorus on the development and progression of NAFLD in rats maintained on a high fat diet. Forty-four six week-old male Sprague-Dawley rats were used for the experiment. Rats were randomly allocated into 5 groups and had free access to water and fed ad libitum either a control diet (20percent protein, 10percent fat by weight) or a high fat diet (20percent protein, 40percent fat by weight) with different concentrations of phosphorus (0.0178, 0.075, 0.15, and 0.3percent) for 8 weeks. Blood was collected for plasma analysis and livers were excised for histology. Results showed that upon feeding male Sprague-Dawley rats phosphate restricted diets (0.0178percent and 0.075percent P); rats had significant weight loss, low intake, and low energy efficiency than rats fed a P sufficient diet. In addition, male Sprague-Dawley rats upon administration of high fat diet tend to induce microvesicular steatosis, and mild macrovesicular steatosis and lobular inflammation. However, effect of P manipulation could not be detected. Although rats developed microvesicular steatosis, mild macrovesicular steatosis, and lobular inflammation; however, effect of P manipulation could not be detected.