Severe COVID-19: insulin- and leptin-resistance in the immune system?!

The brain and immune system have top priority in our survival mechanisms. They should have consistent access to sufficient glucose for energy and as a building block for signaling- and structural molecules. Consequently, these organs are not dependent on insulin for glucose uptake, and therefore employ the insulin-independent GLUT1 for glucose transport. This you may find in textbooks. The question is then: why do some consider Alzheimer as type 3 diabetes and is intranasal insulin investigated as treatment option. Why does the knock-out of the insulin receptor in T-cells affect specific T-cell functions. And why do people with genetic leptin deficiency have low T-cell numbers, low sensitivity to T-cell activation, and low pro-inflammatory cytokine production? Insulin and leptin are emerging as key-players in the link between nutrition and the immune system. Insulin- and leptin-resistance are usually caused by an unhealthy lifestyle. Via their roles in meta-flammation, they are strongly associated with long-term risks of ‘typically Western diseases’, such as diabetes type 2, cardiovascular disease, some cancer types and neurodegenerative diseases. COVID-19 reminds us that insulin- and leptin-resistance are also major risks factors of a poor outcome following acute infection.

Programme Symposium 2022 – 13:30 AM