Gi'day all - for info.....
I attended some of the JDRF "virtual" seminar yesterday. JDRF seminars are excellent, although the "virtual" aspects take the shine off, understandably.
There was some good information about technology developments and exercise. The presentations are, or will soon be, available on-line. If you're interested and did not register, you might still be able to access them if you contact JDRF.
I was very pleased to note that research is progressing well to produce a practical and robust aqueous solution/suspension of Glucagon which is a hormone required to draw glucose (glycogen) from the liver to increase BGL.
A while ago, I raised questions in this forum about why the body couldn't secrete glucagon to stop hypos and why we couldn't self administer glucagon to increase BGL. DQ offered some reasons and together with my own research, I discovered that the glucagon is provided as a powder which must be suspended just prior to injection because it degrades quickly once in suspension. Also, the Alpha cells which produce glucagon are also impaired by T1 or they must wait for a signal from the Beta cells which are destroyed . The latter is counterintuitive for me and I didn't try to understand it further.
Apparently research is well advanced to build pumps with can deliver both glucose and glucagon. -Good news, because I assume this might also reduce the risk of "fatty liver" and remove the need for T1s to eat extra carbo for hypos when there are already stores in the liver. Typically when we eat carbo to raise BGL, much of it will be just stored back into the liver, unless we are using it while its available.
I hope that if I'm incorrect about the glucose cycle (above), T1 professionals in the forum can correct me.
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Jock
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