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Shuimei LIAN, Qian YANG, Ting WANG. TMAO Inhibitors' Effects on Diabetic Sarcopenia in Rats[J]. Journal of Kunming Medical University.
Citation: Shuimei LIAN, Qian YANG, Ting WANG. TMAO Inhibitors' Effects on Diabetic Sarcopenia in Rats[J]. Journal of Kunming Medical University.

TMAO Inhibitors' Effects on Diabetic Sarcopenia in Rats

  • Received Date: 2024-08-26
  •   Objective  To investigate the effects of trimethylamine N-oxide (TMAO) inhibitor on mitochondrial damage, skeletal muscle function, and microvascular senescence in rats with diabetic sarcopenia.  Methods  An animal model of diabetic sarcopenia was established in specific pathogen-free experimental animal (SPF) grade male rats, and intervention was carried out with 3, 3-dimethyl-1-butanol (DMB). The fasting blood glucose, insulin and insulin resistance index of rats in each group were detected. Rope grasping test, gastrocnemius muscle weight, body weight detection; Pathological morphology of the gastrocnemius muscle Detection of mitochondrial membrane potential and ultrastructure Expression of microvascular aging-related proteins matrix metalloproteinase (MMP) -2, monocyte chemoattractant protein (MCP) -1, and transforming growth factor (TGF) -β1.  Results  Compared with the healthy control group, the model group showed significant decreases in insulin level, wire-hanging time, body weight, gastrocnemius muscle weight, gastrocnemius-to-body weight ratio, and mitochondrial membrane potential, along with significant increases in FBG, HOMA-IR, and the expression levels of MMP-2, MCP-1, and TGF-β1 (all P < 0.05). Compared with the model group, the 0.1% DMB group exhibited significant increases in insulin level, wire-hanging time, body weight, gastrocnemius muscle weight, gastrocnemius-to-body weight ratio, and mitochondrial membrane potential, as well as significant decreases in FBG, HOMA-IR, and the expression levels of MMP-2, MCP-1, and TGF-β1 (all P < 0.05).  Conclusion  TMAO inhibitor can reduce FBG and insulin resistance, alleviate mitochondrial damage, and thereby improve skeletal muscle function in rats with diabetic sarcopenia. This effect is presumably achieved by inhibiting the expression of MMP-2, MCP-1, and TGF-β1 to reduce microvascular senescence.
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