Prebiotic effects of commercial apple juice in high-fat diet fed rat.

OBJECTIVES: Apples are one of the most frequently consumed fruits and are effective in preventing lifestyle-related and other diseases. However, few studies have been conducted to evaluate health benefits of processed apple products such as juice. In this study, we analyzed the health benefits of consuming apple juice, focusing on changes in the gut microbiota, which plays an important role in maintaining human health. RESULTS: Rats were fed apple juice ad libitum, and the relative abundances of various gut microbiota in fecal samples were analyzed. In addition, rats treated apple juice were fed with a high-fat diet, and body weight, plasma triglyceride, glucose, and cholesterol levels were measured. The relative abundance of Clostridium cluster XIV did not change with the treatment of apple juice, but the relative abundance of Clostridium cluster IV was significantly decreased. In contrast, the relative abundances of Lactobacillus and Bifidobacterium, which provide benefits to the human body, were significantly increased by 3-fold and 10-fold, respectively, with apple juice consumption. When apple juice-treated rats were fed a high-fat diet, the increase in body weight, liver fat, and blood lipid parameters were all suppressed compared to high-fat alone group. CONCULUSION: This study suggests that the consumption of apple juice changes the gut microbiota, exerts a prebiotic effect, and is effective in improving lifestyle-related diseases.

Green tea extract prevents CPT-11-induced diarrhea by regulating the gut microbiota.

Irinotecan (CPT-11) is an anticancer drug with indications for use in treating various cancers, but severe diarrhea develops as a side effect. We investigated the effects of green tea extract (GTE) on CPT-11-induced diarrhea, focusing on ß-glucuronidase and intestinal UGT1A1. When CPT-11 was administered to rats alone, the fecal water content was approximately 3.5-fold higher in this group than in the control group, and diarrhea developed. The fecal water content in the GTE-treated group was significantly higher than that in the control group, but the difference was smaller than that between the group treated with CPT-11 alone and the control group, and diarrhea improved. When CPT-11 was administered alone, the abundances of Bacteroides fragilis and Escherichia coli, which are ß-glucuronidase-producing bacteria, increased and interleukin-6 and interleukin-1ß mRNA levels in the colon increased, but GTE suppressed these increases. CPT-11 decreased colon UGT1A1 and short-chain fatty acid levels; however, this decrease was suppressed in the GTE-treated group. The findings that GTE decreases the abundance of ß-glucuronidase-producing bacteria and increases colon UGT1A1 levels, thereby decreasing the production of the active metabolite SN-38 in the intestinal tract, indicate that GTE ameliorates CPT-11-induced diarrhea.

CPT-11-Induced Delayed Diarrhea Develops via Reduced Aquaporin-3 Expression in the Colon.

While irinotecan (CPT-11) has a potent anti-cancer effect, it also causes serious diarrhea as an adverse reaction. In this study, we analyzed the pathogenic mechanism of CPT-11-induced delayed diarrhea by focusing on water channel aquaporin-3 (AQP3) in the colon. When rats received CPT-11, the expression level of AQP3 was reduced during severe diarrhea. It was found that the expression levels of inflammatory cytokines and the loss of crypt cells were increased in the colon when CPT-11 was administered. When celecoxib, an anti-inflammatory drug, was concomitantly administered, both the diarrhea and the reduced expression of AQP3 induced by CPT-11 were suppressed. The inflammation in the rat colon during diarrhea was caused via activated macrophage by CPT-11. These results showed that when CPT-11 is administered, the expression level of AQP3 in the colon is reduced, resulting in delayed diarrhea by preventing water transport from the intestinal tract. It was also suggested that the reduced expression of AQP3 might be due to the inflammation that occurs following the loss of colonic crypt cells and to the damage caused by the direct activation of macrophages by CPT-11. Therefore, it was considered that anti-inflammatory drugs that suppress the reduction of AQP3 expression could prevent CPT-11-induced delayed diarrhea.