Drosophila insulin receptor regulates diabetes-induced mechanical nociceptive hypersensitivity.
Drosophila insulin receptor regulates diabetes-induced mechanical nociceptive hypersensitivity.
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DOI：
10.17912/micropub.biology.000456
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发表时间：
2021
影响因子：
--
通讯作者：
Im SH
中科院分区：
文献类型：
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作者：
Dabbara H;Schultz A;Im SH
疼痛性糖尿病神经病变 (PDN) 是糖尿病的主要并发症之一，会导致麻木、刺痛和极度疼痛敏感。了解 PDN 发病机制对于患者治疗非常重要。在这里，我们报告了糖尿病引起的机械伤害性超敏反应的果蝇模型。 2 型糖尿病样病症和多树突感觉神经元中胰岛素受体功能的丧失会导致机械伤害性超敏反应。此外，我们还发现恢复多树突感觉神经元中的胰岛素信号传导可以阻止糖尿病引起的机械伤害性超敏反应。我们的工作强调了伤害性感觉神经元中胰岛素信号传导在调节糖尿病引起的伤害性超敏反应中的关键作用。
Painful diabetic neuropathy (PDN) is one of the predominant complications of diabetes that causes numbness, tingling, and extreme pain sensitivity. Understanding the mechanisms of PDN pathogenesis is important for patient treatments. Here we report Drosophila models of diabetes-induced mechanical nociceptive hypersensitivity. Type 2 diabetes-like conditions and loss of insulin receptor function in multidendritic sensory neurons lead to mechanical nociceptive hypersensitivity. Furthermore, we also found that restoring insulin signaling in multidendritic sensory neurons can block diabetes-induced mechanical nociceptive hypersensitivity. Our work highlights the critical role of insulin signaling in nociceptive sensory neurons in the regulation of diabetes-induced nociceptive hypersensitivities.