The last 18-months has witnessed the collision of the epidemics of diabetes, obesity and COVID-19. The consistent finding of adverse outcomes, from COVID-19, in individuals with diabetes and/or obesity even with hyperglycaemia in the non-diabetic range has focused attention on the metabolic dysfunction that may arise with acute illness and the potential benefit to be gained from glycaemic regulation. Significantly worse outcomes in people with microvascular complications (such as retinopathy or nephropathy) points to endothelial dysfunction as a common mechanism of adverse outcomes. These individuals will be vulnerable to the pro-inflammatory state and microthrombi that ensue with Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2). Trial data have shown that glucocorticoids and anticoagulation address the pro-inflammatory and pro-coagulant pathways. There are emerging trial data targeting other endothelial facets, such as the vasoconstrictive and antioxidant pathways. Another notable feature of the SARS-CoV-2 has been the bidirectionality of response. Unlike the morbidity associated with other infectious agents, such as influenza virus, SARS-CoV-2 itself may promote relative insulin deficiency, ketogenesis and hyperglycaemia in susceptible individuals. The future implications of this are uncertain. In this update, I will highlight how obesity and impaired metabolic health increase complications and mortality in COVID-19 and will summarize the data for metabolic normalisation and mitigation of endothelial cell dysfunction in the acute setting. I will also discuss the consequences of SARS-CoV-2 infection for longer-term metabolic health.
30 Jun 2021 - 01 Jul 2021