Cefalu, William T. Rodgers, Griffin P.
Published in
Cell Metabolism
Diabetes and obesity are associated with greater COVID-19 severity, and certain racial and ethnic groups bear a disproportionate burden of these metabolic diseases. There is a need to focus on SDOH and truly understand how these factors adversely affect an individual’s health and contribute to increasing prevalence of metabolic diseases.
Sadiku, Pranvera Willson, Joseph A. Ryan, Eilise M. Sammut, David Coelho, Patricia Watts, Emily R. Grecian, Robert Young, Jason M. Bewley, Martin Arienti, Simone
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Published in
Cell Metabolism
Neutrophils are required to meet their energy demands at inflamed sites where nutrients may be limited. Sadiku et al. provide evidence of a specialized metabolism that enables neutrophils to utilize glycogen cycling for energy production. This is essential for neutrophil function and survival, and dysregulation is associated with chronic disease st...
Drucker, Daniel J.
Published in
Cell Metabolism
COVID-19 infection produces excess mortality in people with obesity or diabetes. Here we review the epidemiology, susceptibility to infection, pathophysiology, immunology, complications, potential therapeutic options, and response to vaccinations in people with metabolic disorders and SARS-CoV-2 infection.
Cai, Jingjing Li, Haomiao Zhang, Changjiang Chen, Ze Liu, Hui Lei, Fang Qin, Juan-Juan Liu, Ye-Mao Zhou, Feng Song, Xiaohui
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Published in
Cell Metabolism
While corticosteroid therapy is effective in the treatment of patients with severe COVID-19, a quantitative clinical parameter to identify such severity and which patients would respond well to corticosteroids has not been developed. Here, Cai et al. find that a simple blood test that measures the neutrophil-to-leukocyte ratio at admission discrimi...
Donath, Marc Y
Published in
Cell metabolism
Patients with a metabolic syndrome (overweight, diabetes, hypertension, and dyslipidemia) have a particularly bad outcome if infected with SARS-CoV-2. Yu et al. (2020) suggest that insulin therapy itself may promote fatality in patients with COVID-19 and diabetes. Copyright © 2020 Elsevier Inc. All rights reserved.
Corrado, Mauro Edwards-Hicks, Joy Villa, Matteo Flachsmann, Lea J. Sanin, David E. Jacobs, Maaike Baixauli, Francesc Stanczak, Michal Anderson, Eve Azuma, Mai
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Published in
Cell Metabolism
Corrado et al. show that the mitochondrial membrane-specific lipid cardiolipin is required for the metabolic plasticity that is essential for effective CD8+ T cell function. Cardiolipin-deficient CD8+ T cells fail to respond to pathogens and are not able to adapt to nutrient stress.
Yu, Bo Li, Chenze Sun, Yang Wang, Dao Wen
Published in
Cell Metabolism
Type 2 diabetes (T2D) is associated with poor outcome for patients with COVID-19. Here, Yu et al. demonstrated that among 689 patients with T2D from a cohort of 3,305 hospitalized COVID-19 cases, insulin treatment was associated with a significant increase in death rate in patients with COVID-19 and T2D.
Kusmartseva, Irina Wu, Wenting Syed, Farooq Van Der Heide, Verena Jorgensen, Marda Joseph, Paul Tang, Xiaohan Candelario-Jalil, Eduardo Yang, Changjun Nick, Harry
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Published in
Cell Metabolism
Kusmartseva et al. demonstrate preferential ACE2 expression in pancreatic microvascular and ductal structures, suggesting these constitute a more likely target than islet endocrine cells in SARS-CoV-2 infection. This notion was supported by detection of SARS-CoV-2 nucleocapsid protein in ductal epithelium, but not endocrine cells, of pancreata from...
Coate, Katie C. Cha, Jeeyeon Shrestha, Shristi Wang, Wenliang Gonçalves, Luciana Mateus Almaça, Joana Kapp, Meghan E. Fasolino, Maria Morgan, Ashleigh Dai, Chunhua
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Published in
Cell Metabolism
Coate et al. examined expression of canonical SARS-CoV-2 entry proteins ACE2 and TMPRSS2 in the human pancreas and report ACE2 expression in the microvasculature, including islet pericytes, whereas both ACE2 and TMPRSS2 are expressed in some ducts. Conversely, neither protein is detected in β cells, arguing against direct β cell viral infection in ...
Forte, Dorian García-Fernández, María Sánchez-Aguilera, Abel Stavropoulou, Vaia Fielding, Claire Martín-Pérez, Daniel López, Juan Antonio Costa, Ana S.H. Tronci, Laura Nikitopoulou, Efterpi
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Published in
Cell Metabolism
Forte et al. reveal that nestin+ bone marrow stromal cells directly contribute to leukemogenesis and chemotherapy resistance in an in vivo model of acute myeloid leukemia. Nestin+ BMSCs support leukemic stem cells through a dual mechanism of increased bioenergetic capacity through OXPHOS and TCA and glutathione-dependent antioxidant defense.