Covid19 and Diabetes

Some prevously-healthy people, infected with Sars-CoV-2, develop diabetes mellitus. The type 1 version of this condition, is caused by the Islets of Langerhans in the pancreas failing to produce enough insulin. Insulin is a hormone that reduces the blood 'sugar' level by converting glucose into its storage material glycogen ('animal starch'). Separate studies in New York and Sienna have provided some indication of the genesis of the link between Covid19 and diabetes (https://www.theguardian.com/society/2021/sep/29/covid-can-infect-cells-in-pancreas-that-make-insulin-research-shows ). The New York study used tiny clumps of tissue cultured cells, called 'organoids'. This investigation found that cultured pancreatic organoids (along with those of the brain, lung, colon, heart and liver) could be infected by the Covid19 virus. Infection of pancreatic organoids, seemed to change the fate of beta cells (the cells that produce insulin) in the Islets of Langerhans. Beta cells appeared to be reduced in number, the tissue becoming more 'mixed'. The Sienna investigation found that Covid19 attacked pancreatic cells, largely by targeting Angiotensin Converting Enzyme 2 (ACE2) proteins on their surfaces. Infection by the virus also increases the density of ACE2 receptors on the surfaces of insulin-secreting cells. This extra ACE2 made these cells more prone to infection, reducing the subsequent production of the glucose-lowering (hypoglycaemic) hormone. Some debate remains around whether the diabetes, produced by a Covid19 infection, is reversible. The involvement of ACE2 receptors, also possibly accounts for the wide range of symptoms produced by the viral infection. Many organs have the ACE2 receptor.