Sepsis is understood as the result of initiating systemic inflammation derived from an inadequate host response against pathogens. In its acute phase, sepsis is marked by an exacerbated reaction to infection, tissue damage, organ failure, and metabolic dysfunction. Among these, hypoglycemia, characterized by disorders of the gluconeogenesis pathway, is related to one of the leading causes of mortality in septic patients. Recent research has investigated the involvement of sympathetic efferent neuroimmune pathways during systemic inflammation. These pathways can be stimulated by several centrally administered drugs, including Angiotensin-(1–7) (Ang-(1–7)). Therefore, the present study aims to evaluate the effects of central treatment with Ang-(1–7) on hypoglycemia during endotoxemia. For this, male Wistar Hannover rats underwent stereotaxic surgery for intracerebroventricular (i.c.v.) administration of Ang-(1–7) and cannulation of the jugular vein for lipopolysaccharide (LPS) injection. Our results demonstrate that LPS was capable of inducing hypoglycemia and that prior central treatment with Ang-(1–7) attenuated this effect. Our data also show that Ang-(1–7) reduced plasma concentrations of TNF-α, IL-1β, IL-6, and nitric oxide, in addition to the decrease and increase of hepatic IL-6 and IL-10 respectively, in animals subjected to systemic inflammation by LPS, resulting in the reduction of systemic and hepatic inflammation, thus attenuating the deleterious effects of LPS on phosphoenolpyruvate carboxykinase protein content. In summary, the data suggest that central treatment with Ang-(1–7) attenuates hypoglycemia induced by endotoxemia, probably through anti-inflammatory action, leading to reestablishing hepatic gluconeogenesis.

中文翻译：

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中枢血管紧张素-(1-7) 通过减少全身和肝脏炎症来减轻败血症样情况下的低血糖


脓毒症被认为是由于宿主对病原体的反应不足而引发全身炎症的结果。在急性期，脓毒症的特点是对感染、组织损伤、器官衰竭和代谢功能障碍的加剧反应。其中，以糖异生途径紊乱为特征的低血糖是脓毒症患者死亡的主要原因之一。最近的研究调查了全身炎症过程中交感传出神经免疫通路的参与。这些途径可以通过几种中枢给药药物来刺激，包括血管紧张素-(1-7) (Ang-(1-7))。因此，本研究旨在评估Ang-(1-7)中枢治疗对内毒素血症期间低血糖的影响。为此，雄性 Wistar Hannover 大鼠接受了立体定位手术，进行脑室内 (i.c.v.) 注射 Ang-(1-7)，并进行颈静脉插管注射脂多糖 (LPS)。我们的结果表明，LPS 能够诱发低血糖，并且之前使用 Ang-(1-7) 进行集中治疗可以减弱这种作用。我们的数据还表明，Ang-(1–7) 除了分别降低和增加肝脏 IL-6 和 IL-10 外，还降低了 TNF-α、IL-1β、IL-6 和一氧化氮的血浆浓度。在遭受 LPS 全身炎症的动物中，导致全身炎症和肝脏炎症减少，从而减弱 LPS 对磷酸烯醇丙酮酸羧激酶蛋白含量的有害影响。总之，数据表明，Ang-(1-7) 的集中治疗可能通过抗炎作用减轻内毒素血症引起的低血糖，从而重建肝脏糖异生。