Severe COVID-19 associated hyperglycemia is caused by beta cell dysfunction: a prospective cohort study
Jan Gojda1, Kateřina Koudelková2, Anna Ouřadová2
1Department of Internal Medicine, Third Faculty of Medicine, Charles University, and Královské Vinohrady University Hospital, Prague, Czech Republic. jan.gojda@lf3.cuni.cz.
Severe COVID-19 survivors may develop hyperglycemia due to beta cell dysfunction, not insulin resistance. This study in patients without prior diabetes found impaired insulin response, not insulin sensitivity, linked to hyperglycemia post-infection.
Area of Science:
- Endocrinology
- Infectious Diseases
- Metabolic Syndrome
Background:
- COVID-19 (caused by SARS-CoV-2) is linked to new-onset diabetes.
- Mechanisms causing hyperglycemia post-COVID-19 remain unclear.
- This study investigates the roles of insulin resistance and beta cell dysfunction.
Purpose of the Study:
- To determine if hyperglycemia in severe COVID-19 survivors is associated with insulin resistance or beta cell dysfunction.
- To analyze metabolic changes and glucose regulation over six months post-infection.
Main Methods:
- Examined severe COVID-19 survivors without prior diabetes at baseline, 3, and 6 months.
- Utilized oral glucose tolerance tests (OGTT), indirect calorimetry, and corticosteroid use assessment.
- Measured insulin response and sensitivity using indices like DI and ISI; calculated resting energy expenditure (REE).
Main Results:
- Hyperglycemia was present in 17 patients at baseline and 13 at 6 months.
- Insulin sensitivity was similar in hyperglycemic and normoglycemic groups.
- Hyperglycemic patients exhibited lower insulin response (DI), indicating beta cell dysfunction.
Conclusions:
- Severe COVID-19 initially increases REE and insulin resistance, but these effects are temporary.
- Hyperglycemia in these patients is primarily due to beta cell dysfunction, not persistent insulin resistance.
- Insufficient insulin response is the key factor leading to hyperglycemia post-COVID-19.
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