Hello! (Greetings from Finland, sorry my bad English)
A new study about using Victoza on T1. So far Victoza is only used on T2.
Improved HbA1c:
HbA1c decreased significantly at 24 weeks from 6.5 to 6.1% (P=0.02)
Decreased glucose concentrations:
The mean s.d. of glucose concentrations decreased from 56±10 to 26±6 mg/dl (P<0.01) and the coefficient of variation decreased from 39.6±10 to 22.6±7 (P<0.01)
Fall in insulin use:
There was a concomitant fall in the basal insulin from 24.5±6 to 16.5±6 units (P<0.01) and bolus insulin from 22.5±4 to 15.5±4 units (P<0.01)
This is a very interesting article and abstract. If this drug does what they claim it can it could be very beneficial to T1’s. Average BG standard deviation of their 14 subjects dropped by about 50%, reduction in TDD by about 33%, and about 10 lb weight loss seem almost to good to be true. I hope not, though. I will be interested to see what the next, larger study finds.
I am a little confused with the hypothesized activity of Victoza. They are hypothesizing that the drug suppresses post-meal glucagon. I was unaware that T1s released glucagon after a meal? Doesn’t insulin stop the expression and/or release of glucagon? And if glucagon is suppressed for a decent amount of time, then couldn’t it cause insulin-dependents problems if they experience a moderate/severe hypo?
The abstract is too short to answer these questions reasonably for me, but I love the results of the participants.
Victoza is a Glucagon-Like-Peptide (GLP-1) analog. The “incretin” action of GLP-1 is to stimulate insulin release and inhibit glucagon release. Sometimes with diabetes, you can have the opposite effect happen (the so-called anti-incretin effect) when you eat. It is hypothesized that this is why bariatric surgery works in T2s and why the “Chinese Restaurant Effect” happens. Our bodies naturally push out glucagon at the same time as meals as a way of buffering the insulin release. But sometimes, it doesn’t work out well. Whether the slowed digestion is what causes the effect or whether there actually exists an anti-incretin hormone suppressed by GLP-1 is not known. But if if works, who really cares?
Thanks BSC I thought you may chime in. I have never heard of this process. Guess I can believe it is possible, but never would of guessed it. I agree with your sentiments of it it works who really cares, but I am filled with 20+ years of a “cure” is right around the corner. This has lead to an overabundant supply of skepticisim. Any ideas on if Victoza would inhibit a glucagon response when needed, like during a hypo?
The effect of Victoza is only when you eat. I doubt it would have an effect otherwise. And besides, during a hypo, you actually want glucagon since a high level of glucagon signals your liver to dump glucose.
thanks for the link. Slide 12 (showing the 20 mg/dl decrease in standard deviation) of that presentation is beautiful. Answers a lot of my questions. A later slide shows T2s increase glucagon concentration (likely production) after a meal unlike a non-diabetic. I believe a reasonable assumption would be to agree with BSC and conclude that T1s likely increase glucagon concentrations post meal.
Wow! I want to try this stuff. It sounds like it’s actually available in Canada, too, unlike Symlin. Doubt my endocrinologist would prescribe it, though.