Glycemia, Beta-Cell Function and Sensitivity to Insulin in Mildly to Critically Ill Covid-19 Patients

Abstract

Background and objectives: Critically and non-critically ill patients with SARS-CoV-2 infection (Covid-19) may present with higher-than-expected glycemia, even in the absence of diabetes. With this study we aimed to assess glucose, glycemic gap (GlyG) and insulin secretion/sensitivity measures in patients with Covid-19. Materials and Methods: We studied, upon admission, 157 patients with Covid-19 (84: in wards and 73: in intensive care units; ICU); 135 had no history of diabetes. We measured blood glucose upon admission as well as glycated hemoglobin (A1c), plasma insulin and C-peptide. We calculated the GlyG and the Homeostasis Model Assessment 2 (HOMA2) estimates of steady state beta cell function (HOMA2%B) and insulin sensitivity (HOMA2%S). Statistical assessment was done with analysis or the Kruskal-Wallis test. Results: Compared to patients in the wards without diabetes, patients with diabetes in the wards, as well as patients in the ICU (without or with diabetes) had higher admission glycemia. The GlyG was significantly higher in patients without diabetes in the ICU compared to patients without diabetes in the wards, while HOMA2%B based on glucose and insulin was significantly higher in the ICU patients compared to patients in the wards. Of all the parameters, HOMA2%S based on C-peptide/glucose was higher in survivors (n = 133). Conclusions: In our series of patients with Covid-19, a substantial number of patients with and without diabetes had admission hyperglycemia and those who were critically ill may have had compromised insulin secretion and lowered sensitivity to insulin. These findings lend credence to reports of association between Covid-19 and hyperglycemia/secondary diabetes.

Anti-inflammatory adipokines: chemerin, vaspin, omentin concentrations and SARS-CoV-2 outcomes

“…By that date, only a few studies have been investigating the influence of IR on the course of COVID-19 infection. Most of them emphasized the adverse impact of higher IR on the severity and mortality of COVID-19, suggesting the role of chronic inflammation among these groups of patients 56 , 57 . Finucane and Davenport 58 argue that at least in part, a state of IR and elevated insulin levels are driving increased ACE2 expression in lung epithelial cells and, in consequence, aggravating disease severity.…”

Fetuin-A Deficiency but Not Pentraxin 3, FGF-21, or Irisin, Predisposes to More Serious COVID-19 Course

“…To date, only a few studies have investigated the influence of insulin resistance on the course of COVID-19 infection. The adverse impact of higher insulin resistance on the severity and mortality of COVID-19 patients has been proved by most of them, suggesting that chronic inflammation is a key risk factor in this group of patients [41,42]. Finucane and Davenport [43] argue that the state of insulin resistance and elevated insulin levels that are driving increased ACE2 expression in lung epithelial cells are responsible, at least in part, for aggravating disease severity.…”

Novel appearance of hyperglycemia/diabetes, associated with COVID-19

“…In a recent relevant study, of critically and non-critically ill patients with COVID-19, we found that indeed beta cell function (based on glucose and insulin measurements and using the Homeostasis Model Assessment HOMA2 estimate of steady state beta cell function[ 4 ]) was compromised in critically ill patients with COVID-19. Furthermore, these patients showed a high glycemic gap (based on admission glucose and glycated hemoglobin measurements)[ 5 ]. Nevertheless, we acknowledged that on average, 25% of critically ill patients with no history of DM have stress hyperglycemia[ 5 - 7 ], a finding which could obscure the prevalence of hyperglycemia/new-onset DM that could be attributed to COVID-19 per se .…”