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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Metab 2021 ; 33 (11): 2174-2188.e5 Nephropedia Template TP
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Hyperglycemia in acute COVID-19 is characterized by insulin resistance and adipose tissue infectivity by SARS-CoV-2 #MMPMID34599884
Reiterer M; Rajan M; Gomez-Banoy N; Lau JD; Gomez-Escobar LG; Ma L; Gilani A; Alvarez-Mulett S; Sholle ET; Chandar V; Bram Y; Hoffman K; Bhardwaj P; Piloco P; Rubio-Navarro A; Uhl S; Carrau L; Houhgton S; Redmond D; Shukla AP; Goyal P; Brown KA; tenOever BR; Alonso LC; Schwartz RE; Schenck EJ; Safford MM; Lo JC
Cell Metab 2021[Nov]; 33 (11): 2174-2188.e5 PMID34599884show ga
Individuals infected with SARS-CoV-2 who also display hyperglycemia suffer from longer hospital stays, higher risk of developing acute respiratory distress syndrome (ARDS), and increased mortality. Nevertheless, the pathophysiological mechanism of hyperglycemia in COVID-19 remains poorly characterized. Here, we show that hyperglycemia is similarly prevalent among patients with ARDS independent of COVID-19 status. Yet among patients with ARDS and COVID-19, insulin resistance is the prevalent cause of hyperglycemia, independent of glucocorticoid treatment, which is unlike patients with ARDS but without COVID-19, where pancreatic beta cell failure predominates. A screen of glucoregulatory hormones revealed lower levels of adiponectin in patients with COVID-19. Hamsters infected with SARS-CoV-2 demonstrated a strong antiviral gene expression program in the adipose tissue and diminished expression of adiponectin. Moreover, we show that SARS-CoV-2 can infect adipocytes. Together these data suggest that SARS-CoV-2 may trigger adipose tissue dysfunction to drive insulin resistance and adverse outcomes in acute COVID-19.