COVID-19 has proven to be a metabolic disease resulting in adverse outcomes in individuals with diabetes or obesity . Patients infected with SARS-CoV-2 and hyperglycemia suffer from longer hospital stays, higher risk of developing acute respiratory distress syndrome (ARDS), and increased mortality compared to those who do not develop hyperglycemia . Nevertheless, the pathophysiological mechanism (s) of hyperglycemia in COVID-19 remains poorly characterized . Here we show that insulin resistance rather than pancreatic beta cell failure is the prevalent cause of hyperglycemia in COVID-19 patients with ARDS, independent of glucocorticoid treatment . A screen of protein hormones that regulate glucose homeostasis reveals that the insulin sensitizing adipokine adiponectin is reduced in hyperglycemic COVID-19 patients . Hamsters infected with SARS-CoV-2 also have diminished expression of adiponectin . Together these data suggest that adipose tissue dysfunction may be a driver of insulin resistance and adverse outcomes in acute COVID-19.