High fructose intake from soft drinks and sweets is assumed to have a negative impact on human health. Yet in spite of intensive research, the molecular mechanisms of these effects have not been fully elucidated yet, for example, the effect of high fructose intake could be different in normal and obese individuals. Four groups of mice were used in this study: control groups of lean mice and mice with obesity induced by a high-fat diet, then both of these groups with or without fructose administration in drinks. In plasma of each group, triacylglycerol, cholesterol, free fatty acids, alanine aminotransferase, insulin and adiponectin were measured. The expression levels of selected microRNAs (miRNAs) in plasma, the liver, white adipose tissue, brown adipose tissue and subcutaneous adipose tissue were quantified. In both lean and obese mice, high fructose intake increased cholesterol amount in the liver, up-regulated hepatic miR-27a, down-regulated miR-33a in white adipose tissue and increased plasmatic level of miR-21. The effect of high fructose intake on other miRNAs in the liver, plasma and adipose tissues differed in normal and obese mice. Fructose intake led to hepatic hypercholesterolemia and aberrant expression of several miRNAs participating in lipid metabolism, adipocytes differentiation and nonalcoholic fatty liver disease promotion. The effect of fructose on miRNAs expression differed in normal and obese mice. Nevertheless, plasmatic miR-21, which was induced by fructose in both lean and obese mice, may be considered as a potential biomarker of excessive fructose intake.
Keywords: Fructose; MicroRNA; Obesity; adipose tissue; lipid metabolism; miR-21.
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