Last class (October 22) we finished learning about glycolysis and went over a case study involving a boy who kept having syncopal episodes in school. The doctor ordered a fasting fructose tolerance test, showing that his blood glucose dropped. This actually reminded me of my own personal syncopal episodes in early middle school as a result of hypoglycemia, although for different reasons for the one in the case study. After going to my family doctor, I too had a sort of glucose fasting test in the hospital. I can’t remember the name of the specific test, but I do know that I periodically had my blood drawn and was connected to an IV, so maybe it was some sort of tolerance test on my metabolic breakdown of glucose.
What they found was that my asthma medication containing synthetic glucocorticoids was suppressing my natural production of cortisol in my adrenal glands. While we haven’t discussed this hormone at length in biochemistry, it does play a role in regulating blood glucose levels through a few mechanisms. Cortisol can act on the liver, with high cortisol levels increasing gluconeogenesis and decreasing glycogen synthesis. Gluconeogenesis is basically the reverse of glycolysis, producing glucose from glucogenic amino acids, lactate, or glycerol 3- phosphate. It can also influence muscles with muscle cells decreasing glucose uptake and consumption and increasing protein degradation in response to cortisol signaling. This supplies gluconeogenesis with glucogenic amino acids. Lastly, cortisol acts on the pancreas to decrease insulin and increase glucagon, which would be a good response to hypoglycemia due to these hormones stimulating the liver to release stored glucose to raise blood sugar levels.