The mortality rate of diabetics who are hospitalized with Covid-19 is significant. Alarmingly individuals that survive Coid-19 can present with a diagnosis of diabetes after hospitalization including people who were not necessarily presenting with risk factors for the disease. Because the Corona Virus can enter cells of the pancreas, the intestine, the liver and fat tissue, maintaining normal sugar metabolism is problematic. However, somatostatin is still the target as it too is placed strategically in all of these vulnerable areas which Covid-19 seeks out. It is widely known that somatostatin inhibits insulin in the pancreas; and it nullified a hefty spike in insulin is the result. In this case, insulin degrading enzyme isn’t helpful as somatostatin is its substrate, leading to its inability to do its job.
Somatostatin would usually control levels of cortisol as it blocks ACTH in its secretion (ACTH being the hormone that stimulates the production of cortisol). Without this mechanism in place, cortisol levels can escalate to unprecedented heights. In this scenario on one hand it is helpful. Cortisol can promote glucose sourced from the liver to match the high insulin. Therefore it seems a destructive phase can be neutralized. However, in saying this, prolonged high levels of cortisol will eventually burn out the beta cells in the Islets of Langerhans (insulin baring cells).
Developing diabetes as a result from Covid-19 is a possibility. A loss of life because an individual has diabetes and contracts Covid-19 is also a high risk factor. Glucagon is also still in the mix trying to bring stability.
Overall somatostatin needs further investigation in the fight against Cov19. Is it somewhat depleted or are the receptors compromised or something else? Whatever the case, a better understanding of it with Covid 19 may be warranted.
https://www.today.com/health/can-covid-19-cause-diabetes-what-you-need-know-t208654
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