Age-Related Structural Susceptibility of Rat Liver Parenchyma to HFCS-55-Induced Injury Under Distinct Energy Conditions: A Semi-Quantitative Histological Study

Background: High-fructose corn syrup (HFCS) is widely used as a sweetener in processed foods and beverages, and excessive intake has been associated with histopathological alterations and hepatic injury.However, the age-dependent effects of chronic HFCS-55 consumption on hepatic fibrosis and structural liver alterations remain incompletely understood.This study aimed to investigate the age-dependent effects of HFCS-55 consumption on the development of hepatic fibrosis and histopathological alterations of the liver under different feeding regimens.Materials and Methods: Young (2-month-old) and aged (15-month-old) male Sprague-Dawley rats were divided into three groups within each age category (n = 10 per group): control (standard chow and water ad libitum), HFCS plus restricted chow (10 g/day), and HFCS plus restricted chow (20 g/day).HFCS was administered as an 11% solution during the dark period.The feeding protocol lasted 16 weeks.At the end of the experiment, liver tissues were collected and evaluated using hematoxylin and eosin, Masson's trichrome, and Direct Red 80 staining to assess structural damage and collagen deposition.Results: HFCS-fed groups, particularly the HFCS + restricted chow (20 g/day) groups in both young and aged rats, exhibited hepatocellular degeneration, sinusoidal dilatation, increased collagen deposition, and mild-to-moderate fibrosis compared to controls.A statistically significant increase in hepatic injury and fibrosis scores was observed only in the HFCS + restricted chow (20 g/day) groups compared to their respective controls (p < 0.05).These changes were more pronounced in aged rats.Conclusion: Chronic consumption of HFCS-55-containing beverages was associated with age-dependent hepatic injury and fibrosis in rats.These findings suggest that both aging and high fructose intake may contribute to the progression of hepatic damage.However, because the present study was limited to histopathological evaluation, further studies incorporating molecular analyses (e.g., markers of oxidative stress, inflammation, and apoptosis) are warranted to elucidate the underlying mechanisms.