Santos Andrey, Magro Daniéla Oliveira, Evangelista-Poderoso Rosana, Saad Mario José Abdalla
Department of Internal Medicine-FCM, State University of Campinas-UNICAMP, Campinas, SP, Brazil.
Department of Surgery, Faculty of Medical Sciences, State University of Campinas-UNICAMP, Campinas, SP, Brazil.
Diabetol Metab Syndr. 2021 Mar 1;13(1):23. doi: 10.1186/s13098-021-00639-2.
Our understanding of the pathophysiology of the COVID-19 manifestations and evolution has improved over the past 10 months, but the reasons why evolution is more severe in obese and diabetic patients are not yet completely understood.
In the present review we discuss the different mechanisms that may contribute to explain the pathophysiology of COVID-19 including viral entrance, direct viral toxicity, endothelial dysfunction, thromboinflammation, dysregulation of the immune response, and the renin-angiotensin-aldosterone system.
We show that the viral infection activates an integrated stress response, including activations of serine kinases such as PKR and PERK, which induce IRS-1 serine phosphorylation and insulin resistance. In parallel, we correlate and show the synergy of the insulin resistance of COVID-19 with this hormonal resistance of obesity and diabetes, which increase the severity of the disease. Finally, we discuss the potential beneficial effects of drugs used to treat insulin resistance and diabetes in patients with COVID-19.
在过去10个月里，我们对新冠病毒疾病（COVID-19）临床表现及病情演变的病理生理学的理解有所进步，但肥胖和糖尿病患者病情演变更严重的原因尚未完全明确。
在本综述中，我们讨论了可能有助于解释COVID-19病理生理学的不同机制，包括病毒进入、直接病毒毒性、内皮功能障碍、血栓炎症、免疫反应失调以及肾素-血管紧张素-醛固酮系统。
我们发现病毒感染激活了一种综合应激反应，包括丝氨酸激酶如PKR和PERK的激活，这些激酶诱导胰岛素受体底物-1（IRS-1）丝氨酸磷酸化和胰岛素抵抗。同时，我们关联并展示了COVID-19的胰岛素抵抗与肥胖和糖尿病的这种激素抵抗之间的协同作用，这会增加疾病的严重程度。最后，我们讨论了用于治疗COVID-19患者胰岛素抵抗和糖尿病的药物的潜在有益作用。
