Ayaka Sekita1, Yukako Okazaki2, Tetsuyuki Katayama3. 1. Faculty of Human Life Sciences, Fuji Women's University, Ishikari, Japan. 2. Faculty of Human Life Sciences, Fuji Women's University, Ishikari, Japan. Electronic address: yokazaki@fujijoshi.ac.jp. 3. Institution of Life Sciences and Nutrition, Kita-ku, Japan.
Abstract
OBJECTIVES: The aim of this study was to investigate the effect of phytic acid (PA) on fatty liver and gut microflora in rats fed a high-sucrose (HSC) diet. METHODS: Three groups of rats were fed a high-starch (HSR) diet or an HSC diet with or without 1.02% sodium PA for 12 d. We evaluated hepatic weight, total lipids, and triacylglycerol (TG) levels, the activities and expression of hepatic lipogenic enzymes (glucose-6-phosphate dehydrogenase, malic enzyme 1, and fatty acid synthetase), and fecal microflora. RESULTS: The HSC diet significantly increased hepatic total lipids and TG levels, and the activities and expression of the hepatic lipogenic enzymes compared with the HSR diet. These upregulations were clearly suppressed by dietary PA. Consumption of PA elevated the fecal ratio of Lactobacillus spp. and depressed the ratio of Clostridium cocoides, and suppressed the elevation in the ratio of C. leptum induced by the HSC diet. CONCLUSION: This work showed that dietary PA ameliorates sucrose-induced fatty liver through reducing the expression of hepatic lipogenesis genes and modulates gut microflora in rats.
OBJECTIVES: The aim of this study was to investigate the effect of phytic acid (PA) on fatty liver and gut microflora in rats fed a high-sucrose (HSC) diet. METHODS: Three groups of rats were fed a high-starch (HSR) diet or an HSC diet with or without 1.02% sodium PA for 12 d. We evaluated hepatic weight, total lipids, and triacylglycerol (TG) levels, the activities and expression of hepatic lipogenic enzymes (glucose-6-phosphate dehydrogenase, malic enzyme 1, and fatty acid synthetase), and fecal microflora. RESULTS: The HSC diet significantly increased hepatic total lipids and TG levels, and the activities and expression of the hepatic lipogenic enzymes compared with the HSR diet. These upregulations were clearly suppressed by dietary PA. Consumption of PA elevated the fecal ratio of Lactobacillus spp. and depressed the ratio of Clostridium cocoides, and suppressed the elevation in the ratio of C. leptum induced by the HSC diet. CONCLUSION: This work showed that dietary PA ameliorates sucrose-induced fatty liver through reducing the expression of hepatic lipogenesis genes and modulates gut microflora in rats.