SHERYL M SATO
$372,799
WEILL MEDICAL COLL OF CORNELL UNIV
New York
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Coronavirus disease of 2019 (COVID-19) is a worldwide pandemic that quickly grew from the end of 2019 to more than 5.6 million confirmed cases as of late May 2020. The number of cases is approaching 1.7 million with over 100,000 deaths in our country. Within the United States, there is tremendous regional variability in the prevalence of COVID-19 with New York State and specifically the New York City metro area being particularly hard hit. The demographic risk factors for adverse outcomes such as need for mechanical ventilation and mortality in COVID-19 include diabetes and obesity. Hyperglycemia in COVID-19 is associated with poor outcomes; however, the mechanism for hyperglycemia remains unknown. Emerging evidence show that SARS-CoV-2 could infect cells outside of the nasopharynx and lungs. ACE2 is a coreceptor for SARS-CoV-2 and is expressed on pancreatic islet cells, including beta cells. We hypothesize that SARS-CoV-2 directly infects beta cells to cause beta cell dysfunction and acute hyperglycemia. We propose to define the physiological mechanism of hyperglycemia in COVID-19 patients assessing samples from a large biobank. Understanding the mechanism for hyperglycemia may translate into clinical treatments that may improve care of COVID-19 patients.