Intake of phytic acid and myo-inositol lowers hepatic lipogenic gene expression and modulates gut microbiota in rats fed a high-sucrose diet.

Dietary phytic acid (PA) was recently reported by our group to suppress hepatic lipogenic gene expression and modulate gut microbiota in rats fed a high-sucrose (HSC) diet. The present study aimed to investigate whether the modulatory effects of PA depend on the dietary carbohydrate source and are attributed to the myo-inositol (MI) ring of PA. Male Sprague-Dawley rats were fed an HSC or a high-starch (HSR) diet with or without 1.02% sodium PA for 12 days. Subsequently, the rats were fed the HSC diet, the HSC diet containing 1.02% sodium PA or an HSC diet containing 0.2% MI for 12 days. The HSC diet significantly increased the hepatic triglyceride (TG) concentration as well as the activity and expression of hepatic lipogenic enzymes compared with the HSR diet. The increases were generally suppressed by dietary PA with a concomitant increase in the fecal and cecal ratios of Lactobacillus spp. In rats fed the HSR diet, PA intake did not substantially affect the factors associated with hepatic lipid metabolism or gut microbiota composition. The effects of MI intake were similar to that of PA intake on hepatic lipogenesis and gut microbiota in rats fed the HSC diet. These results suggest that dietary PA downregulates hepatic lipogenic gene expression and modulates gut microbiota composition in rats fed an HSC diet but not in rats fed an HSR diet. The MI ring of PA may be responsible for the effects of PA intake on hepatic lipogenic gene expression and gut microbiota.

Dietary phytic acid prevents fatty liver by reducing expression of hepatic lipogenic enzymes and modulates gut microflora in rats fed a high-sucrose diet.

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.

Consumption of lily bulb modulates fecal ratios of firmicutes and bacteroidetes phyla in rats fed a high-fat diet.

It has been recently suggested a high ratio of fecal Firmicutes and reduction in the Bacteroidetes in obese animals. This study investigated the effect of dietary lily bulb (LB) on fecal Firmicutes and Bacteroidetes in rats fed a high-fat (HF) diet. In experiment 1, rats were fed an HF diet with or without 7% raw (R) or steamed (S) LB. In experiment 2, rats were fed the HF diet with or without 7% RLB, 0.9% ethanol extract of LB, or 6.1% ethanol extract residue of LB. In experiment 1, fecal Firmicutes was reduced and Bacteroidetes was increased in both the RLB and SLB groups. In experiment 2, the fecal Firmicutes/Bacteroidetes ratio was not affected by the ethanol extract or ethanol extract residue of LB. These results suggest that LB in its entirety modulates colonic microflora, regardless of heat treatment.