The liver dumps extra glucose for a variety of reasons like stress or monthly hormones.
For a non-D person, I’ve read that the liver stops dumping glucose when they eat because the alpha cells in the pancreas signal that it’s not necessary. If my alpha cells aren’t working properly because, perhaps, they got killed off with my beta cells, does that mean that my liver is always dumping glucose when I don’t need it (such as when I’m eating)?
Someone on TuD said that Afrezza reinstigates this signalling to the liver, so that the liver stops dumping while the Afrezza is active. They linked the article below.
Maybe this idea only applies to people with type 2 diabetes, but I’m a little confused by the whole thing. The person suggested that taking Metformin messes with all this signalling so it’d be better for people with T2 to start Afrezza, rather than Metformin.
I recently got a script for Metformin because I think I’m experiencing increased insulin resistance at night between around 7 pm until 2 am. I was planning to try it for a month to see if it helps. I’m also hoping it might help with my weight in a number of ways, but that thinking may be too optimistic. If it doesn’t help with the weight, then I’m going to be switching to Levemir or Lantus so that I can vary my basal dose more (e.g. days when I exercise).
However, my doctor really didn’t like the idea of prescribing Metformin. He said that my basal dose was low enough that he didn’t think it would help me at all, and that it might put me at risk of lows. He said that it seemed pointless since my A1c is so good… The visit was actually very frustrating for a variety of reasons, and I think I’m going to be switching endos within the next year.
I suppose I’m posting this topic because I’m trying to understand how all these drugs interact with each other and which effects of these drugs apply to people who’ve had type 1 for a long time. I’m trying to understand all the risks involved with adding a new medication. I’ve only ever used insulin to treat my diabetes.
For instance, is there a chance that I do still have some alpha cells left that have protected me from really severe lows (before my cgm I had a few prolonged ones during the night)? If so, by taking Metformin, will I be harming these cells? If I go off a month after starting, can I expect that everything would go back to how it was before or could these cells be permanently harmed?
Also, for those of you with T1 and on Metformin, is the risk of lows only the result of you needing to lower your basal dose? Or will there be a higher risk overall? I’m a little confused about the whole idea of an extra risk of lows. It seems like that risk would decrease once you’d lowered your basal dose to the right dose while on Metformin.
Thanks for reading! I appreciate any insights you experts have to offer.