Spinal cord injury (SCI) is an independent risk factor for type 2 diabetes, and may induce insulin resistance that leads to this disease. Studies have shown that greater phosphoinositide 3-kinase (PI3K) activation in the hypothalamus leads to activation of the anti-inflammatory pathway, and the anti-inflammatory reflex may protect against insulin resistance and type 2 diabetes. However, the importance of this phenomenon in type 2 diabetes pathogenesis after SCI remains elusive. In the present study, the expression of c-Fos in the hypothalamus of rats with SCI was elevated, and the hypothalamus injury was observer following SCI. Then we showed that SCI could induce increased levels of blood glucose and glucose tolerance in rats. Also, we found that SCI could damage the liver, adipocyte and pancreas, and led to lipid position in liver. Western blots were used to detect the level of PI3K and p-Akt in the hypothalamus, and the results showed a significant downregulation of PI3K and p-Akt after SCI. Furthermore, to verify the activity of the PI3K signaling pathway, immunofluorescence was used to examine the expression of neurons positive for p-S6 (a marker of PI3K activation) after SCI. The results showed that the expression of p-S6-positive neurons decreased after SCI. In addition, the effect of SCI on peripheral inflammation was also investigated. Following SCI, the serum levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 increased. Collectively, our results suggest abnormality in glucose metabolism after SCI, and demonstrate that SCI may impair activation of the PI3K signaling pathway in the hypothalamus. The reduced activity of the PI3K signaling pathway in the hypothalamus may lead to peripheral inflammation, which might be the mechanism underlying the development of insulin resistance and type 2 diabetes following SCI.

脊髓损伤 (SCI) 是 2 型糖尿病的独立危险因素，并可能诱发导致这种疾病的胰岛素抵抗。研究表明，下丘脑中更大的磷酸肌醇 3-激酶 (PI3K) 激活导致抗炎途径的激活，并且抗炎反射可以预防胰岛素抵抗和 2 型糖尿病。然而，这种现象在 SCI 后 2 型糖尿病发病机制中的重要性仍然难以捉摸。在本研究中，SCI 大鼠下丘脑中 c-Fos 的表达升高，下丘脑损伤是 SCI 后观察者。然后我们发现 SCI 可以诱导大鼠血糖水平和葡萄糖耐量升高。此外，我们发现 SCI 会损害肝脏、脂肪细胞和胰腺，并导致肝脏中的脂质位置。Western blots检测下丘脑PI3K和p-Akt水平，结果显示SCI后PI3K和p-Akt显着下调。此外，为了验证 PI3K 信号通路的活性，使用免疫荧光检查 SCI 后 p-S6（PI3K 激活的标志物）阳性神经元的表达。结果表明，脊髓损伤后p-S6阳性神经元的表达降低。此外，还研究了 SCI 对外周炎症的影响。SCI 后，血清肿瘤坏死因子-α、白细胞介素 (IL)-1β 和 IL-6 水平升高。总的来说，我们的结果表明 SCI 后葡萄糖代谢异常，并证明 SCI 可能损害下丘脑 PI3K 信号通路的激活。