Diabetes, obesity, and insulin resistance in COVID-19: molecular interrelationship and therapeutic implications.
Diabetes, obesity, and insulin resistance in COVID-19: molecular interrelationship and therapeutic implications.
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DOI：
10.1186/s13098-021-00639-2
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发表时间：
2021-03-01
影响因子：
4.8
通讯作者：
Saad MJA
中科院分区：
文献类型：
--
作者：
Santos A;Magro DO;Evangelista-Poderoso R;Saad MJA
在过去的10个月里，我们对COVID-19的病理生理学表现和进化的认识有所提高，但肥胖和糖尿病患者进化更严重的原因尚不完全清楚。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、免疫反应失调和肾素-血管紧张素-醛固酮系统。我们发现病毒感染激活了一个综合的应激反应，包括激活丝氨酸激酶，如PKR和PERK，诱导IRS-1丝氨酸磷酸化和胰岛素抵抗。与此同时，我们将COVID-19的胰岛素抵抗与肥胖和糖尿病的激素抵抗相关联并显示出协同作用，从而增加了疾病的严重程度。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。
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.
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