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新型冠状病毒在胰腺中的存在及 COVID-19 患者胰岛功能受损。

SARS-CoV-2 in the pancreas and the impaired islet function in COVID-19 patients.

机构信息

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.

Key Laboratory of Antibody Techniques, National Health Commission, Department of Immunology, Nanjing Medical University, Nanjing, People's Republic of China.

出版信息

Emerg Microbes Infect. 2022 Dec;11(1):1115-1125. doi: 10.1080/22221751.2022.2059400.

Abstract

Diabetes mellitus (DM) is one of the most common underlying diseases that may aggravates COVID-19. In the present study, we explored islet function, the presence of SARS-CoV-2 and pathological changes in the pancreas of patients with COVID-19. Oral glucose tolerance tests (OGTTs) and the C-peptide release test demonstrated a decrease in glucose-stimulated C-peptide secretory capacity and an increase in HbA1c levels in patients with COVID-19. The prediabetic conditions appeared to be more significant in the severe group than in the moderate group. SARS-CoV-2 receptors (ACE2, CD147, TMPRSS2 and neuropilin-1) were expressed in pancreatic tissue. In addition to SARS-CoV-2 virus spike protein and virus RNA, coronavirus-like particles were present in the autophagolysosomes of pancreatic acinar cells of a patient with COVID-19. Furthermore, the expression and distribution of various proteins in pancreatic islets of patients with COVID-19 were altered. These data suggest that SARS-CoV-2 in the pancreas may directly or indirectly impair islet function.

摘要

糖尿病(DM)是可能加重 COVID-19 的最常见基础疾病之一。在本研究中,我们探讨了 COVID-19 患者的胰岛功能、SARS-CoV-2 的存在和胰腺的病理变化。口服葡萄糖耐量试验(OGTT)和 C 肽释放试验表明,COVID-19 患者的葡萄糖刺激 C 肽分泌能力下降,HbA1c 水平升高。与中度组相比,严重组的糖尿病前期情况更为显著。胰腺组织中表达了 SARS-CoV-2 受体(ACE2、CD147、TMPRSS2 和神经纤毛蛋白-1)。除了 SARS-CoV-2 病毒刺突蛋白和病毒 RNA 外,COVID-19 患者的胰腺腺泡细胞的自噬溶酶体中还存在冠状病毒样颗粒。此外,COVID-19 患者胰岛中各种蛋白质的表达和分布发生改变。这些数据表明,胰腺中的 SARS-CoV-2 可能直接或间接损害胰岛功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a831/9037197/21d91ba69e3b/TEMI_A_2059400_F0001_OC.jpg

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