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Ganglioside GM3 synthase depletion reverses neuropathic pain and small fiber neuropathy in diet-induced diabetic mice

机译：神经节苷脂GM3合酶耗竭可逆转饮食诱发的糖尿病小鼠的神经性疼痛和小纤维神经病变

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Small fiber neuropathy is a well-recognized complication of type 2 diabetes and has been shown to be responsible for both neuropathic pain and impaired wound healing. In previous studies, we have demonstrated that ganglioside GM3 depletion by knockdown of GM3 synthase fully reverses impaired wound healing in diabetic mice. However, the role of GM3 in neuropathic pain and small fiber neuropathy in diabetes is unknown. Determine whether GM3 depletion is able to reverse neuropathic pain and small fibers neuropathy and the mechanism of the reversal. We demonstrate that GM3 synthase knockout and the resultant GM3 depletion rescues the denervation in mouse footpad skin and fully reverses the neuropathic pain in diet-induced obese diabetic mice. In cultured dorsal root ganglia from diet-induced diabetic mice, GM3 depletion protects against increased intracellular calcium influx in?vitro. These studies establish ganglioside GM3 as a new candidate responsible for neuropathic pain and small fiber neuropathy in diabetes. Moreover, these observations indicate that systemic or topically applied interventions aimed at depleting GM3 may improve both the painful neuropathy and the wound healing impairment in diabetes by protecting against nerve end terminal degeneration, providing a disease-modifying approach to this common, currently intractable medical issue.
机译：小纤维神经病是一种公认​​的2型糖尿病并发症，已被证明可引起神经性疼痛和伤口愈合不良。在以前的研究中，我们已经证明，通过敲低GM3合酶来减少神经节苷脂GM3可以完全逆转糖尿病小鼠伤口愈合的损害。但是，GM3在糖尿病的神经性疼痛和小纤维神经病变中的作用尚不清楚。确定GM3耗竭是否能够逆转神经性疼痛和小纤维神经病变及其逆转机理。我们证明，GM3合酶基因敲除和由此产生的GM3耗竭挽救了小鼠足垫皮肤的神经支配，并完全扭转了饮食诱发的肥胖糖尿病小鼠的神经性疼痛。在饮食诱导的糖尿病小鼠的培养的背根神经节中，GM3的消耗可防止体外细胞内钙内流的增加。这些研究将神经节苷脂GM3确立为负责糖尿病中神经性疼痛和小纤维神经病变的新候选药物。此外，这些观察结果表明，旨在预防GM3的系统或局部应用的干预措施可通过防止神经末梢退行性变来改善糖尿病患者的疼痛性神经病和伤口愈合障碍，从而为该常见的当前棘手的医学问题提供疾病缓解方法。

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