Animal study demonstrates that a high-sucrose diet triggers hepatic oxidative stress and MMP-9 activation in mice, suggesting a mechanism for liver damage and fibrogenesis.
Excessive sucrose consumption is associated with various metabolic disorders, including obesity, diabetes, and liver dysfunction. Although oxidative stress is a well-established mechanism contributing to these conditions, its effects on matrix metalloproteinase (MMP) activity in the liver remain poorly understood. This study evaluated the impact of a high-sucrose diet on oxidative stress, MMP-2 and MMP-9 activities, insulin signaling and collagen deposition in the liver of Swiss mice. Male Swiss mice (protocol no. 7,422,050,723) were divided into 2 groups with 16 animals each—control and high-sucrose diet—and were fed for 4 weeks. Liver samples were collected for histomorphological analysis of steatosis, inflammatory infiltrates, and collagen deposition, as well as for biochemical evaluation of antioxidant enzyme activity, oxidative stress markers, MMP activity, and AKT phosphorylated at serine 473. The high-sucrose diet induced metabolic imbalance, steatosis, and inflammatory infiltration, accompanied by oxidative stress in the liver, evidenced by reduced catalase activity (CAT) and glutathione levels (GSH), along with increased protein carbonyls (PCO) and thiobarbituric acid reactive substances (TBARS) levels. Additionally, MMP-9 activity and collagen deposition were higher in mice fed the high-sucrose diet. Notably, AKT phosphorylation at Ser-473 residue was reduced, indicating impaired insulin signaling. These findings suggest that a high-sucrose diet induces hepatic oxidative stress, disrupts insulin signaling, and promotes MMP-9 activation, potentially contributing to liver histopathological changes and dysfunction.
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Passos et al. (2026) studied this question.
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