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BACKGROUND: Microplastics (MPs) are small particles of plastic ([less than or equal to] 5 mm in diameter). In recent years, oral exposure to MPs in living organisms has been a cause of concern. Leaky gut syndrome (LGS), associated with a high-fat diet (HFD) in mice, can increase the entry of foreign substances into the body through the intestinal mucosa. OBJECTIVES: We aimed to evaluate the pathophysiology of intestinal outcomes associated with consuming a high-fat diet and simultaneous intake of MPs, focusing on endocrine and metabolic systems. METHODS: C57BL6/J mice were fed a normal diet (ND) or HFD with or without polystyrene MP for 4 wk to investigate differences in glucose tolerance, intestinal permeability, gut microbiota, as well as metabolites in serum, feces, and liver. RESULTS: In comparison with HFD mice, mice fed the HFD with MPs had higher blood glucose, serum lipid concentrations, and nonalcoholic fatty liver disease (NAFLD) activity scores. Permeability and goblet cell count of the small intestine (SI) in HFD-fed mice were higher and lower, respectively, than in ND-fed mice. There was no obvious difference in the number of inflammatory cells in the SI lamina propria between mice fed the ND and mice fed the ND with MP, but there were more inflammatory cells and fewer anti-inflammatory cells in mice fed the HFD with MPs in comparison with mice fed the HFD without MPs. The expression of genes related to inflammation, long-chain fatty acid transporter, and [Na.sup.+]/glucose cotransporter was significantly higher in mice fed the HFD with MPs than in mice fed the HFD without MPs. Furthermore, the genus Desulfovibrio was significantly more abundant in the intestines of mice fed the HFD with MPs in comparison with mice fed the HFD without MPs. Muc2 gene expression was decreased when palmitic acid and microplastics were added to the murine intestinal epithelial cell line MODE-K cells, and Muc2 gene expression was increased when IL-22 was added. DISCUSSION: Our findings suggest that in this study, MP induced metabolic disturbances, such as diabetes and NAFLD, only in mice fed a high-fat diet. These findings suggest that LGS might have been triggered by HFD, causing MPs to be deposited in the intestinal mucosa, resulting in inflammation of the intestinal mucosal intrinsic layer and thereby altering nutrient absorption. These results highlight the need for reducing oral exposure to MPs through remedial environmental measures to improve metabolic disturbance under high-fat diet conditions. https://doi.org/10.1289/EHP11072, Introduction Over the past few decades, the use of plastics has increased dramatically. (1) The production, use, and consumption of plastics, which has been ongoing since the 1950s, has caused [...]

Royal jelly (RJ) is a naturally occurring substance synthesized by honeybees and has various health benefits. Herein, we focused on the medium-chain fatty acids (MCFAs) unique to RJ and evaluated their therapeutic efficacy in treating non-alcoholic fatty liver disease (NAFLD). We examined db/m mice that were exclusively fed a normal diet, db/db mice exclusively fed a normal diet, and db/db mice fed varying RJ quantities (0.2, 1, and 5%). RJ improved NAFLD activity scores and decreased gene expression related to fatty acid metabolism, fibrosis, and inflammation in the liver. RJ regulated innate immunity-related inflammatory responses in the small intestine and decreased the expression of genes associated with inflammation and nutrient absorption transporters. RJ increased the number of operational taxonomic units, the abundance of Bacteroides, and seven taxa, including bacteria that produce short-chain fatty acids. RJ increased the concentrations of RJ-related MCFAs (10-hidroxy-2-decenoic acid, 10-hydroxydecanoic acid, 2-decenedioic acid, and sebacic acid) in the serum and liver. These RJ-related MCFAs decreased saturated fatty acid deposition in HepG2 cells and decreased the gene expression associated with fibrosis and fatty acid metabolism. RJ and RJ-related MCFAs improved dysbiosis and regulated the expression of inflammation-, fibrosis-, and nutrient absorption transporter-related genes, thereby preventing NAFLD. [ABSTRACT FROM AUTHOR]

This study investigated the effects of miso, a traditional fermented soybean food in Japan, on muscle mass atrophy. Eight week old male C57BL/6J mice were fed high fat/high sucrose diet with or without miso for 12 weeks. A miso diet increased soleus muscle weights ( p <0.05) and reduced intraperitoneal glucose tolerance and insulin tolerance ( p <0.05). The miso diet downregulated the Tnfα and Ccl2 expression, related to inflammation, and Trim63 and Fbxo32 expression, related to muscle atrophy, in the soleus muscle ( p <0.05). The miso diet increased short-chain fatty acids levels, including acetic, propanoic, and butanoic acids, in the feces, serum, and soleus muscle ( p <0.05). According to the LEfSe analysis, the miso diet increased family Prevotellaceae, family Christensenellaceae, family Dehalobacterium, family Desulfitibacter; family Deferribacteraceae, order Deferribacterales, class Deferribacteres; and family Gemmatimonadaceae, order Gemmatimonadetes, and class Gemmatimonadales, whereas the miso diet decreased family Microbacteriaceae, order Micrococcales, class Actinobacteria, and family Lactobacillaceae. Miso suppressed high fat/high sucrose diet induced impaired glucose tolerance, low muscle strength, and muscle atrophy by improving dysbiosis and increasing short-chain fatty acids production and provides new insights into the preventive effects of fermented foods on sarcopenia., Competing Interests: YH has received personal fees from Sanofi K.K., Mitsubishi Tanabe Pharma Co., Daiichi Sankyo Co., Ltd., and Novo Nordisk Pharma Ltd., outside the submitted work. TS has received personal fees from MSD K.K., Astellas Pharma Inc., Ono Pharma Co., Ltd., Kissei Pharma Co., Ltd., Mitsubishi Tanabe Pharma Co., Kowa Pharma Co., Ltd., Taisho Toyama Pharma Co., Ltd., Kyowa Hakko Kirin Co., Ltd., Takeda Pharma Co., Ltd., Sanofi K.K., Novo Nordisk Pharma Ltd., and Eli Lilly Japan K.K., outside the submitted work. EU has received grants from the Japanese Study Group for Physiology and Management of Blood Pressure (Grant number: 4024). Donated Fund Laboratory of Diabetes therapeutics is an endowment department, supported with an unrestricted grant from Ono Pharmaceutical Co., Ltd., and received personal fees from MSD K.K., Takeda Pharmaceutical Co., Ltd., Astellas Pharma Inc., Kowa Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., AstraZeneca plc, Novo Nordisk Pharma Ltd., Taisho Toyama Pharmaceutical Co., Ltd., Kyowa Hakko Kirin Company Ltd., Daiichi Sankyo Co., Ltd., and Sumitomo Dainippon Pharma Co., Ltd., outside the submitted work. MH has received grants from Mitsubishi Tanabe Pharma Co., Sumitomo Dainippon Pharma Co., Ltd., Asahi Kasei Pharma, Sanofi K.K., Takeda Pharmaceutical Co., Ltd., Astellas Pharma Inc., Daiichi Sankyo Co., Ltd., Eli Lilly Japan K.K., Novo Nordisk Pharma Ltd., Nippon Boehringer Ingelheim Co., Ltd., and Kyowa Kirin Co., Ltd., outside the submitted work. MF has received grants from Taisho Pharma Co., Ltd., Ono Pharma Co., Ltd., Daiichi Sankyo Co., Ltd., Sanwa Kagaku Kenkyusho Co., Ltd., Nippon Boehringer Ingelheim Co., Ltd., Astellas Pharma Inc., Kissei Pharma Co., Ltd., Sanofi K.K., MSD K.K., Takeda Pharma Co., Ltd., Teijin Pharma Ltd., Eli Lilly Japan K.K., Novo Nordisk Pharma Ltd., Sumitomo Dainippon Pharma Co., Ltd., Abbott Japan Co., Ltd., Mitsubishi Tanabe Pharma Co., Kyowa Hakko Kirin Co., Ltd., Johnson & Johnson K.K. Medical Co., Terumo Co., Nippon Chemiphar Co., Ltd., and Kowa Pharmaceutical Co., Ltd.; and received personal fees from Taisho Pharma Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Eli Lilly Japan K.K., Mitsubishi Tanabe Pharma Co., AstraZeneca plc, Nippon Boehringer Ingelheim Co., Ltd., Sanwa Kagaku Kenkyusho Co., Ltd., Astellas Pharma Inc., Kissei Pharma Co., Ltd., Daiichi Sankyo Co., Ltd., Bayer Yakuhin, Ltd., Kyowa Kirin Co., Ltd., Kowa Pharma Co., Ltd., Novo Nordisk Pharma Ltd., Medtronic Japan Co., Ltd., Ono Pharma Co., Ltd., Mochida Pharma Co., Ltd., Takeda Pharma Co., Ltd., Abbott Japan Co., Ltd., Arkley Inc., MSD K.K., Teijin Pharma Ltd., Sanofi K.K., and Nipro Co., outside the submitted work., (Copyright © 2024 JCBN.)

We studied the effect of cleaning and cooking on the residues of flutolanil, fenobucarb, silafluofen and buprofezin in rice. The rice had been sprayed in a paddy field in Wakayama city, with 3 kinds of pesticide application protocols: spraying once at the usual concentration of pesticides, repeated spraying (3 times) with the usual concentration of pesticides and spraying once with 3 times the usual concentration of pesticides. The residue levels of pesticide decreased during the rice cleaning process. Silafluofen, which has a higher log Pow value, remained in the hull of the rice. Fenobucarb, which has a lower log Pow value, penetrated inside the rice. The residue concentration of pesticide in polished rice was higher than that in pre-washed rice processed ready for cooking. During the cooking procedure, the reduction of pesticides in polished rice was higher than that in brown rice.