“Dietary reference intakes for Japanese” is one of the authorized guidelines published by the Ministry of Health, Labour and Welfare of Japan. It is unique as a comprehensive guideline for dietary intake and nutrition. The latest issue, “Dietary reference intakes for Japanese (2015) ”, comprises 344 pages, or 440 pages including the reference section attached to the last volume. There are a few revisions of the figures. On the other hand, its role as a guideline is emphasized, and the application methods, especially those from a theoretical viewpoint, are described in detail in this revised edition. The present article summarizes the “Dietary reference intakes for Japanese (2015) ” with some discussion of its academic and practical significance.
The effects of cooked rice flours on cecal fermentation in rats were examined. The rice flours used were Yukihikari and Honoka 224, which have the genealogy of the rice cultivar Hokkaido, and Kirara 397 and Shimahikari, which have the genealogy of the cultivar Koshihikari. Rats were fed either a control diet or one of the experimental diets each containing one of the four rice flours as a starch source. The animals were fed the diet at 300 g/kg for 28 days. In comparison with the control group, the rats fed Honoka 224 were found to have a significantly lower cecal pH, their cecal concentrations of acetate and total short-chain fatty acids (SCFA) tended to be higher (acetate: p＝0.067, total-SCFA: p＝0.050) , and their immunogloblin A (IgA) and ammonia nitrogen concentrations were significantly higher. In the rats fed Yukihikari, the cecal acetate and total SCFA concentrations were significantly higher. In the rats fed Shimahikari, the cecal mucin concentration tended to be higher and the cecal IgA concentration was significantly higher. Collectively, these findings suggest that consumption of cooked rice improves cecal fermentation, and that this effect is influenced by the genealogy of the rice.
The prevalence of non-alcoholic fatty liver disease (NAFLD) , which is a risk factor for development of type 2 diabetes mellitus, has increased dramatically in Japan. An effective program for prevention and amelioration of NAFLD is therefore required. In this study, we examined the preventive effects of exercise timing (before or after meals) and exercise duration (6 or 9 weeks) on fatty liver induced by a high-fat diet (HFD) in mice. Accumulation of liver triacylglycerol was prevented by a longer duration of exercise, although the timing of exercise had no significant effect. We then investigated the hepatic expression of mRNAs related to liver lipid synthesis, including peroxisome proliferator-activated receptor γ, a transcription factor induced by an HFD, and its target gene. These mRNAs were significantly suppressed by the exercise training, irrespective of exercise duration. Additionally, the expression of sterol regulatory element-binding protein-1c, a major regulator of de novo lipogenesis in the liver, and its target genes were also suppressed by long-term exercise. These results suggest that long-term exercise is highly effective for prevention of fatty liver and that the same degree of benefit can be obtained from both pre- and post-prandial exercise.
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