Elsevier

Nutrition

Volume 32, Issue 6, June 2016, Pages 720-722
Nutrition

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

https://doi.org/10.1016/j.nut.2016.01.003Get rights and content

Highlights

  • We examined the effect of dietary phytate on fatty liver and gut microflora in rats.

  • Phytate prevents fatty liver and modulates gut microflora in rats fed a high-sucrose diet.

  • Dietary phytate downregulates the gene expression of hepatic lipogenic enzymes.

  • Phytate increases Lactobacillus spp. and decreases Clostridium spp. in rat feces.

  • We report the relations among phytate intake, fatty liver, and gut microflora in rats.

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.

Introduction

Phytic acid (PA; myo-inositol hexaphosphoric acid), a ubiquitous plant component, has been traditionally considered an antinutrient [1]. However, it has been demonstrated that dietary PA prevents fatty liver caused by a high-sucrose (HSC) diet in rats [2]. To our knowledge, no information exists on whether suppression of hepatic activities of lipogenic enzymes by PA intake in rats fed the HSC diet is associated with changes in gene expression of hepatic lipogenic enzymes.

When PA is administered as a dietary supplement, it is suggested that undigested PA or partially digested inositol phosphates accumulate in the gastrointestinal tract of monogastric animals such as humans and rodents [3], [4]. The presence of undigested products of PA in the gut may have beneficial effects on the gut microflora, similar to those associated with dietary fiber or oligosaccharides [5]. Several lines of evidence suggest a role for the gut microbiota in the etiology of nonalcoholic fatty liver disease [6]. It is possible that the preventive effect of PA on fatty liver due to the HSC diet may be related to modulation of gut microflora.

It has been demonstrated that dietary PA modulates characteristics of the colonic environment in rats fed a high-fat diet [7]. The present study was conducted to examine whether dietary PA affects the gene expression of hepatic lipogenic enzymes and to investigate the relation between anti-fatty liver activity of PA and gut microflora in rats fed the HSC diet.

Section snippets

Materials and methods

Male Sprague Dawley rats were purchased, maintained, and housed as previously described [8]. The rats were assigned to three groups of six rats each randomized by weight. Compositions of the high-starch (HSR), the HSC and the HSC plus 1.02% dodecasodium PA (Sigma Chemical Co., St Louis, MO, USA) diets were described elsewhere [2]. Previous studies indicated that at around 1%, PA perfectly prevents fatty liver due to the HSC diet or xenobiotic intake in rats [2], [9], [10]. Experimental diets

Results

Final body weight did not differ among the three groups (Table 1). Food intake was slightly increased in rats fed the HSC diet compared with those fed the HSR diet. Compared with the HSR diet, the HSC diet significantly increased the levels of hepatic weight, total lipids and triacylglycerol, and the activities and gene expression of hepatic lipogenic enzymes (P < 0.05; Table 1). These increases were clearly suppressed by dietary PA (P < 0.05; Table 1). PA intake elevated the fecal ratio of

Discussion

To our knowledge, this is the first study to report that the preventive effect of dietary PA on fatty liver induced by the HSC diet is mediated through the downregulation of expression of hepatic lipogenic enzymes. As previously explained, gut microflora including Lactobacillus spp. and Clostridium spp. regulates hepatic lipogenesis and fat storage [6], [14], [15]. This study also provides the first evidence that dietary PA increases the fecal ratio of Lactobacillus spp. and depresses the

Conclusion

PA doses used in this study were relatively higher than in human consumption via food, because some human populations may consume up to ∼1 g/d of PA [1]. However, we previously found that supplementation with as little as ∼0.05% PA in the diet could downregulate the high levels of hepatic lipids and hepatic activities of lipogenic enzymes due to the HSC diet in rats [10]. It is possible that dietary PA may be useful to improve fatty liver induced by an HSC, mineral-sufficient diet in humans.

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This research was supported in part by a Grant-in-Aid (no.15, G-9, 2015) from The Tojuro Iijima Foundation for Food Science and Technology in Japan. YO designed and supervised the study. AS and YO performed the animal experiments. All three authors contributed to the analysis of data and the interpretation of the results, wrote the draft of the manuscript, and critically reviewed it. The authors have no conflicts of interest to declare.

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