Evaluates liver damage and oxidative stress from monk fruit sweetener in rats, suggesting safety concerns for long-term use.
Background Non-nutritive sweeteners (NNS) such as monk fruit sweetener (MFS) are increasingly adopted as sugar alternatives due to their high sweetening potency and low caloric content. Despite their widespread use, the metabolic and hepatic safety profiles of these agents remain underexplored. This study investigates the effect of MFS on the liver histology and key biochemical markers; alanine aminotransferase (ALT), aspartate aminotransferase (AST), and malondialdehyde (MDA) in adult male adult Wistar rats. Methods Twenty adult male Wistar rats were assigned into four groups (n=5/group). Group A served as the control, while Groups B, C, and D received 100, 150, and 200 mg/kg body weight of MFS orally for four weeks. Liver histology was studied using H&E and Masson trichrome stained sections of the liver. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and malondialdehyde (MDA) were assessed. Data obtained was analyzed using one way ANOVA. Results MFS administration resulted in significant elevations in ALT (p=0.001) and MDA (p=0.002), consistent with hepatocellular injury and increased oxidative stress. Although AST levels were elevated, the change did not reach statistical significance. Histological evaluation demonstrated dose-dependent hepatic alterations, including hepatocellular vacuolation, necrosis, sinusoidal and central vein congestion, and increased collagen deposition. Conclusions Exposure to MFS was associated with biochemical and structural hepatic alterations in a dose-dependent manner, raising concerns regarding its hepatic safety under conditions of sustained use. Further mechanistic and long-term studies are warranted to clarify the translational relevance of these findings in humans.
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