Related references
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Endocrinology & Metabolism
Paul M. M. McKeigue et al.
Summary: Using national register data and virology laboratory data, this study found that there was no association between SARS-CoV-2 infection and an increase in the incidence of type 1 diabetes. Although there was an increase in type 1 diabetes incidence in children during the pandemic, it was not caused by SARS-CoV-2 infection.
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Clemens Kamrath et al.
Summary: The study found a significant increase in the incidence of type 1 diabetes in children during the COVID-19 pandemic in Germany, with the peak incidence of diabetes occurring approximately 3 months after the peak of the COVID-19 pandemic. The underlying causes are yet unknown, but more likely to be indirect effects of the pandemic rather than direct effects.
Article
Endocrinology & Metabolism
Andrea Laurenzi et al.
Summary: This study aimed to assess whether dysglycemia diagnosed during COVID-19 pneumonia could become a potential public health problem after the infection is resolved. The research found that COVID-19-associated dysglycemia is unlikely to be a lasting public health problem, thereby cautioning against alarmist claims on the risk of diabetes after COVID-19 pneumonia.
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Endocrinology & Metabolism
Sara J. Cromer et al.
Summary: Newly diagnosed diabetes mellitus (NDDM) associated with COVID-19 is more common in younger patients and less common in non-Hispanic White race/ethnicity. NDDM is characterized by lower glucose levels and higher inflammatory markers. It is associated with lower insulin requirements, longer length of stay, and intensive care unit admission, but not with death. Approximately half of NDDM patients experience regression of diabetes.
JOURNAL OF DIABETES AND ITS COMPLICATIONS
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Article
Cell Biology
Verena van der Heide et al.
Summary: In this study, comprehensive single-cell analysis of SARS-CoV-2-infected human pancreatic islets revealed that the infection is strictly dependent on the ACE2 receptor and targets various pancreatic cell types. However, the infection is limited and non-cytopathic, causing only mild cellular perturbations and inflammatory responses. Similar outcomes were observed with endemic coronaviruses. Further evaluation is needed to determine if COVID-19-induced damage to the pancreas and immunological changes increase the risk of diabetes.
Article
Endocrinology & Metabolism
Riddhi Das Gupta et al.
Summary: This study demonstrates progressive recovery of beta-cell secretion in new-onset A-beta + ketosis-prone diabetes (KPD) provoked by COVID-19 infection in Indian adults. These patients have a distinct profile from Type 1A diabetes. Meticulous follow-up involving C-peptide estimations can guide treatment and prevent unnecessary use of insulin.
JOURNAL OF DIABETES AND ITS COMPLICATIONS
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Article
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Ziyad Al-Aly et al.
Summary: This study analyzed the US Department of Veterans Affairs national healthcare databases to investigate the occurrence of Long COVID and death risk after breakthrough SARS-CoV-2 infection. The findings showed that vaccination significantly reduced the risk of death and post-acute sequelae but did not eliminate them completely. These results underscore the importance of further research on prevention and post-acute care for breakthrough infections.
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Endocrinology & Metabolism
Yan Xie et al.
Summary: This study found an increased risk and burden of incident diabetes and antihyperglycaemic use in people with COVID-19 in the post-acute phase compared to a contemporary control group. The risks and burdens of post-acute outcomes were related to the severity of the acute phase of COVID-19.
LANCET DIABETES & ENDOCRINOLOGY
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Medicine, General & Internal
Emma Rezel-Potts et al.
Summary: The incidence of cardiovascular disease and diabetes mellitus increases in the acute and post-acute phases after COVID-19, but declines in the long-term phase. Short-term cardiovascular complications after COVID-19 mainly include pulmonary embolism, atrial arrhythmias, and venous thromboses.
Letter
Medicine, General & Internal
Rayzel Shulman et al.
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Endocrinology & Metabolism
Luming Wan et al.
Summary: Zhong et al. demonstrate that the protein GP73 stimulates hepatic glucose production and is induced in response to infection with SARS-CoV-2 in vitro and in vivo, proposing a molecular mechanism underlying hyperglycemia associated with COVID-19.
Article
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Kikuko Amo-Shiinoki et al.
Summary: The study reveals that there is a significant presence of dedifferentiation in diabetic islets in Japanese individuals, leading to beta cell loss. As the disease progresses, the proportion of dedifferentiated cells increases substantially, indicating that islet remodeling with dedifferentiation is the underlying cause of beta cell failure during the course of diabetes progression in humans.
Article
Gastroenterology & Hepatology
Sanjay Pandanaboyana et al.
Summary: Patients with acute pancreatitis and coexistent SARS-CoV-2 infection are at higher risk of developing severe pancreatitis, acute respiratory distress syndrome (ARDS), prolonged hospital stays, and increased 30-day mortality.
Article
Cell Biology
Chien-Ting Wu et al.
Summary: There is evidence suggesting a complex relationship between COVID-19 and diabetes, with SARS-CoV-2 being able to directly induce beta cell killing and this effect being rescued by NRP1 inhibition.
Article
Cell Biology
Xuming Tang et al.
Summary: Recent clinical data suggest a correlation between COVID-19 and diabetes. This study found SARS-CoV-2 viral antigen in pancreatic beta cells, leading to the possibility of cell transdifferentiation. Infection with SARS-CoV-2 can cause changes in cell fate, providing new insights into the pathomechanisms of COVID-19.
Article
Cell Biology
Moritz Reiterer et al.
Summary: The study found that hyperglycemia is common among patients with ARDS, and in patients with both ARDS and COVID-19, insulin resistance is the main cause of hyperglycemia. COVID-19 patients have lower levels of adiponectin, and SARS-CoV-2 may infect adipocytes, leading to dysfunction of adipose tissue.
Article
Multidisciplinary Sciences
Charlotte Steenblock et al.
Summary: This study comprehensively analyzed pancreatic tissues from COVID-19 patients and found detectable SARS-CoV-2 viral infiltration in beta-cells, potentially contributing to metabolic dysregulation. Even in the absence of overt new-onset diabetes, viral infection of pancreatic beta-cells may lead to varying degrees of metabolic abnormalities.
NATURE COMMUNICATIONS
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Article
Endocrinology & Metabolism
Laura Montefusco et al.
Summary: Patients with COVID-19 may experience hyperglycaemia, insulin resistance, and abnormal glucose metabolism, with these glycaemic abnormalities potentially persisting for at least 2 months after recovery. Further research into metabolic abnormalities in the context of long COVID is warranted.
Article
Endocrinology & Metabolism
Janis A. Mueller et al.
Summary: The study shows that SARS-CoV-2 can infect and impact insulin secretion in human pancreatic cells, potentially contributing to metabolic dysregulation observed in COVID-19 patients.
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Cell Biology
Irina Kusmartseva et al.
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Daniela Fignani et al.
FRONTIERS IN ENDOCRINOLOGY
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JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
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