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BACKGROUND@#Microplastics (MPs) are small fragments from any type of plastic formed from various sources, including plastic waste and microfibers from clothing. MPs degrades slowly, resulting in a high probability of human inhalation, ingestion and accumulation in bodies and tissues. As its impact on humans is a prolonged event, the evaluation of its toxicity and influence on human health are critical. In particular, MPs can enter the human digestive system through food and beverage consumption, and its effect on the human colon needs to be carefully examined. @*METHODS@#We monitored the influence of small MPs (50 and 100 nm) on human colon cells, human colon organoids and also examined their toxicity and changes in gene expression in vivo in a mouse model. @*RESULTS@#The data suggested that 5 mg/mL concentrations of 50 and 100 nm MPs induced a[ 20% decrease in colon organoid viability and an increase in the expression of inflammatory-, apoptosis- and immunity-related genes. In addition, in vivo data suggested that 50 nm MPs accumulate in various mouse organs, including the colon, liver, pancreas and testicles after 7 d of exposure. @*CONCLUSION@#Taken together, our data suggest that smaller MPs can induce more toxic effects in the human colon and that human colon organoids have the potential to be used as a predictive tool for colon toxicity.
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BACKGROUND: Food restriction has been reported to ameliorate diabetes and obesity. In this study, we examined the effects of the food restriction on phenotypes of TALLYHO/JngJ (TH) mouse, a recently developed diabetic model animal. METHODS: 3 week-old TH mice were divided into 2 groups (n = 20 each for food-restricted (THR) and free-fed (THF)) and THR mice were fed the same amount of food as normal control mice (C57BL/6, n = 20). Body weight was weekly monitored till 14 weeks of age. The half of animals were sacrificed at 8 weeks of age, and liver, kidney, and fat weight were measured. The histopathology of liver and brown fat tissues and mRNA expression of leptin in adipose tissue were analyzed. The oral glucose tolerance test and insulin resistance test was done at 14 weeks of age. The plasma concentrations of glucose, free fatty acid, triglyceride, cholesterol and leptin were analyzed. RESULTS: The THR mice had lower body weights than the THF mice, similar to C57BL/6 mice, with reduced fat deposition in liver and brown fat tissue. The plasma levels of glucose, triglyceride and free fatty acid were decreased in the THR group. The THR mice, however, carried more fat than normal mice, with increased plasma leptin concentration and leptin mRNA expression in fats and no alteration in plasma cholesterol levels. Furthermore, the THR mice revealed glucose intolerance with impaired after-meal insulin secretion and slight insulin resistance CONCLUSION: The food restriction apparently ameliorated the obesity and diabetic phenotypes of TH mice. However, plasma concentration of cholesterol were not improved in THR mice with increased adiposity index and glucose intolerance, suggesting the genetically prone tendency of obesity and diabetes development in TH mice possibly with an impairment in cholesterol metabolism.