Furthermore, the steatotic liver, if infected by the virus, could contribute to hyperglycaemia and hyperinsulinaemia and could also contribute to organ dysfunction in COVID-19 via dysregulated production of lipids, cytokines and hepatokines 9. SARS-CoV-2 is thought to infect hepatocytes, resulting in hepatic dysfunction. Such dysregulated metabolic conditions characterized by hyperglycaemia, hyperinsulinaemia and subclinical inflammation are commonly observed in people with visceral obesity and reduced gluteofemoral adipose tissue mass, and particularly in people with non-alcoholic fatty liver disease 9. In this respect, increased levels of glucose were found to facilitate viral replication and cytokine production in monocytes, and glycolysis was found to sustain SARS-CoV-2-induced monocyte response and viral replication 8. In addition, hyperglycaemia might promote this process. Furthermore, insulin-resistant hyperinsulinaemia could be an important factor in enabling SARS-CoV-2 to infect adipose tissue 6. In addition, in humans, higher levels of ACE2 expression were observed in visceral adipose tissue as compared with subcutaneous adipose tissue, and ACE2 expression was found to increase with age 7. Interestingly, it might not be adipose tissue per se, but rather specifically lipid-laden adipocytes that enable the virus to infect adipose tissue and to replicate 5. What, therefore, is the big picture about adiposity and severe COVID-19? There is ample evidence that adipose tissue is an important target for SARS-CoV-2 (refs. These data suggest that SARS-CoV-2 infection of adipocytes is dependent on a sufficient availability of lipids within the cells 5. Furthermore, the authors found that ACE2 expression was strongly induced upon adipocyte differentiation, and that inhibition of lipolysis in adipocytes strongly reduced viral replication. Importantly, this infection was particularly pronounced in lipid-laden cells and the authors found SARS-CoV-2 RNA in adipose tissue of people with active SARS-CoV-2 infection and COVID-19 who had obesity and overweight, but not those who were lean. In support of this conclusion, a 2022 study found that SARS-CoV-2 could infect adipocytes but not preadipocytes 5. On the basis of these data and their findings that insulin resistance is the main cause for hyperglycaemia in patients with severe COVID-19, the authors concluded that SARS-CoV-2 might induce adipose tissue dysfunction, resulting in insulin resistance and adverse outcomes in acute COVID-19 (ref. In addition, this study found that SARS-CoV-2 could directly infect human and mouse adipocytes. For example, a 2021 study found viral RNA in the adipose tissue of SARS-CoV-2-infected Syrian hamsters, together with reduced secretion of the anti-inflammatory and cardiometabolically protective hormone adiponectin compared with non-infected animals 4. A role of adipose tissue in mediating severe outcomes of SARS-CoV-2 infection has also been proposed by other researchers.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |