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Life sciences · Journal article
Medical and Clinical Chemistry · September 30, 2026
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Introduction. Excessive fructose consumption has become a major public health concern in developed countries, including Ukraine. Chronic high fructose intake is associated with obesity and contributes to the development of metabolic dysfunction-associated steatotic liver disease (MASLD), diabetes mellitus, arterial hypertension, dementia, accelerated aging, and certain malignancies, largely due to excessive adipose tissue accumulation. The aim of the study – to investigate the development of fructose-induced metabolic dysfunction-associated steatotic liver disease in male and female rats and to evaluate the associated metabolic alterations. Research Methods. A rat model of fructose-induced metabolic dysfunction-associated steatotic liver disease was established by daily administration of a 20 % fructose solution for two months. Liver injury was assessed by determining serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) activities, as well as alpha-fetoprotein concentration. Insulin resistance was evaluated using the intraperitoneal glucose tolerance test (IPGTT). Lipid metabolism was assessed by measuring serum total lipids, cholesterol, and triacylglycerols. Metabolic alterations were evaluated according to body weight dynamics and liver and visceral fat weight coefficients. Statistical analysis was performed using methods of variation statistics. Results and Discussion. Chronic fructose administration resulted in a significant increase in ALT, AST, and GGT activities, serum alpha-fetoprotein concentration, and liver weight coefficient compared with the control animals. The area under the glycemic curve increased significantly in both male and female rats, indicating the development of insulin resistance. Fructose-treated rats also developed dyslipidemia, gained body weight, and accumulated visceral fat, with these changes being more pronounced in males. At the same time, biochemical manifestations of liver injury were more pronounced in females. Conclusions. Daily consumption of a 20 % fructose solution for two months induced obesity in rats of both sexes through visceral fat accumulation, which was more pronounced in males. Chronic fructose intake promoted the development of metabolic dysfunction-associated steatotic liver disease and dyslipidemia in both sexes. The severity of liver injury was sex-dependent and greater in female rats. Insulin resistance was confirmed by the intraperitoneal glucose tolerance test.