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September 2, 2026Journal of Biochemical and Molecular ToxicologyOpen Access

Inhibition of Tropomyosin Receptor Kinase B Signaling Alters Hepatic Mitochondrial Enzyme Activity and Oxidative Stress in Mice With Sucrose‐Induced Insulin Resistance

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Authors

ABAkın BodurHZHüseyin Çınar ZihniKKKatip Korkmaz

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Overview

Preclinical study reveals that TrkB receptor inhibition alters hepatic mitochondrial activity and reduces oxidative stress in sucrose-fed mice, indicating a regulatory role in liver metabolism.

Key Points

  • To examine the impact of pharmacological TrkB receptor inhibition using ANA-12 on hepatic mitochondrial enzyme activities and oxidative stress markers in mice with sucrose-induced insulin resistance.
  • Male C57BL/6J mice were allocated into four groups: Control, Sucrose (35% solution), Sucrose+DMSO, and Sucrose+ANA-12 (0.5 mg/kg).
  • Following a 16-week dietary sucrose intervention, mice received daily intraperitoneal injections of ANA-12 or vehicle during the final 21 days.
  • Hepatic activities of cytochrome c oxidase, superoxide dismutase, and catalase, alongside malondialdehyde, serum metabolic parameters, and BDNF levels, were quantified.
  • Sucrose feeding significantly elevated body weight, serum insulin, HOMA-IR, cholesterol, and hepatic malondialdehyde, while reducing hepatic BDNF levels.
  • ANA-12 treatment produced statistically significant decreases in serum leptin and ceramide levels compared to the Sucrose+DMSO group, although reductions in body weight and HOMA-IR were not statistically significant.
  • TrkB inhibition with ANA-12 significantly increased hepatic cytochrome c oxidase activity, altered superoxide dismutase activity, and decreased hepatic malondialdehyde concentrations relative to vehicle controls.

Cite This Study

Bodur et al. (2026) studied this question.

synapsesocial.com/papers/6a97e29ec562ede874ec6cbahttps://doi.org/10.1002/jbt.71104
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