I am approved and will be restarting GLP-1 (Victoza) soon. It’s been 8 years since I lost GLP-1 access due to change of diagnosis from T2 to T1. Any exeprience or references on starting point for decreasing basal and bolus insulin (via pump) will be appreciated. 20% reduction in basal seems to be the recommended starting point, but that is likely based on T2D. I’ll be counting clicks and starting out slow.
If you have endogenous insulin production it gets tricky because then you don’t have the “impaired glucagon response” which those of us who do not produce insulin have. Insulin reduces the production of glucagon and that reduces the release of glucose from the liver, decreasing any basal requirement.
The bottom line is to fast for 24 hours then monitor total insulin intake until you flatline; that’s your basal.
The gotcha is that if your exercise levels are highly variable, as mine are, then the answer is only correct for that exercise level. Exercise increases insulin sensitivity, or rather increased exercise does.
My own approach has been to deliberately underdose then correct. Particular if I’m expecting higher levels of exercise I drop my basal massively (50%) then just correct. It’s very easy to use basal to cover bolus and that’s fine so long as we don’t stop eating… Hence the fasting test.
Interesting you say that you have impaired glucagon response because you are type 1. I’ve been type 1 for almost 40 years, I have zero insulin production for t least 35 years. However I dump glycogen quite easily and often.
I have a strong predawn spike in the morning at 330 Am.
And I get a spike from adrenaline, like if someone cuts me off in traffic. I can go from 100 to 250 in less than a min.
And my doctor tells me to not correct a high like this because it will naturally go down, but it doesn’t for me, I have to correct it.
1 Like
I’m glad you asked… I’ve used Victoza in the past, but it was before I had a CGM so I didn’t know what it was doing! Now I’m on Ozempic - my dose just doubled from 0.5 to 1.0 and it’s been a horrible rollercoaster the past few days. I’m here for the advice 
About two years ago, something about my system’s regulation or use of glucose seemed to change such that TIR suffered and hypoglycemia incidentgs increased. “Impaired glucagon response” is, possilby, a candidate as a cause of my perceived loss of glucose regulation. It could also have been somehow related to back pain that led me to a spinal fusion operation.
Allison,
When I first started Byetta (only GLP-1 at the time) those many years ago, I wish someone had told me to cut down on food intake in advance. It could have saved quite a bit in GI symptoms and to better weight loss experience.
This time I will be starting slower, counting clicks for lower starting dose and smaller step increases.
Thanks! I have to say, Victoza was a game-changer for me (in 2015). I didn’t have any issues with GI effects, thankfully. Later my endo switched me to Trulicity since it’s only once per week instead of daily. I really did not like the auto-injector, so was switched to Ozempic and here I am now. Down 40ish pounds and better blood sugar control!
The alpha cells respond to lots of different things and they work in I think most if not all T1s. The impairment is that their production of glucagon is not turned off by the production of insulin in the beta cells.
Recent research (a couple of years ago) which I might have referenced here showed that to cause the alpha cells to shut down it was necessary to expose them to a very high local concentration of insulin. The concentration was such that it would only occur naturally in the islets (clusters) of alpha and beta cells than Langerhans identified in the pancreas.
The alpha cells do also go into overdrive when our BG drops to dangerous levels; I’ve experienced that several times over the last 50 years, but the feedback mechanism for normal BG regulation involves the beta cell insulin production.
In the absence of beta cells that last mechanism is absent. So far as I know all the others are present. This is what I understand to be the “impaired glucagon response” and the “impairment” is that it continues all the time leading to our requirement for a basal dose of insulin.
More detail is here:
Glucagon Physiology - Endotext - NCBI Bookshelf.
If the link doesn’t show the highlight look for the heading “GLUCAGON SECRETION”.
That book is from 2019, before the more recent research; the authors knew that somehow BG levels regulated glucagon production but didn’t have the essential piece of information that this regulation went via the insulin production of beta cells (I believe that was just a hypothesis in 2019).
Your point is the first sentence:
Glucagon is secreted in response to hypoglycemia, prolonged fasting, exercise and protein-rich meals (10)
To that list add “stress”.
@William7 's question is driven by the third sentence (I added the italics):
Stimulatory regulators of glucagon release include hypoglycemia, amino acids and the gut hormone glucose-dependent insulinotropic peptide (GIP), whereas hyperglycemia and GLP-1 inhibit glucagon release.
If that is correct and the inhibition occurs in the absence of the beta cells then T1s would expect a reduced basal requirement from GLP-1 along with people endogenous insulin production. This paper:
Glucagon-like peptide 1 receptor agonists in type 1 diabetes mellitus - PubMed
Specifically (from the “summary”, about the middle of the paragraph):
GLP-1 RAs have a unique mechanism of action in T1DM, addressing alpha cell dysfunction and thereby suppressing inappropriate glucagon secretion.
Note that once again the alpha cells are getting blamed for “inappropriate glucagon secretion”; the paper explicitly says the cause is “alpha cell dysfunction” not the absence of beta cells. This is fairly typical of inappropriate assumptions made by scientists 
The conclusion section may apply to @William7 I added the emphasis:
Patients who have detectable C-peptide and/or are overweight or cannot achieve glycemic goals without hypoglycemia have been found to benefit the most from GLP-1 RA therapy.
To me that suggests those of us with fully developed T1 and a tightly controlled diet probably won’t benefit that much from GLP-1 agonists. In fact I hadn’t seen that before; I’d assumed the opposite would be the case since people with detectable C-peptide have “less impaired” glucagon regulation.
John Bowler, 2025
My TDD generally goes down by 60% when I’m on mounjaro, but the way to test your change would be to do a basal test for 24 hrs I believe (assuming you use a cgm)
Does your insulin drop by 60% because you eat less with no appetite, or is it just increasing insulin sensetivity