Thanks for posting this…it’s always interesting to read about the new medications and studies. Here are a few snippets that jumped out at me:
“The 12-week trial investigated the efficacy and safety of 800 mg of TTP399 compared with placebo in 85 people with type 1 diabetes on optimized insulin therapy.”
“Based upon this analysis, people treated with TTP399 achieved a statistically-significant placebo-subtracted reduction in HbA1c of 0.32% (p=0.001). Patients taking TTP399 experienced a 0.21% reduction in HbA1c, while patients taking placebo experienced a 0.11% increase in HbA1c, from a mean study baseline HbA1c of 7.6% following a multi-week insulin optimization period prior to the administration of study treatment.”
I don’t understand how “optimized insulin therapy” resulted in a mean baseline HbA1c of 7.6%. It seems like the mean would be in the 6’s if the insulin optimization was truly optimal. Not sure what to make of this, but interesting article nonetheless. Particularly the “no side effects” conclusion…I am guessing that side effects keep a lot of people off Metformin.
They consider any a1c less than 8 to be meeting goals generally and thus “optimal”
Of course we as individuals might not agree, but that’s the lens most research seems to focus through
John, I don’t think this is what we would want.
What this will do is, after you eat, it will cause your liver to store the glucose. It seems that this will prioritize glycogenesis by the liver, which is where glucose is converted and stored as glycogen.
Fine and good if you are sitting on a couch. Not so good if you have a hockey game coming up!
If you have activity, after you eat you want glycolysis, not glycogenesis. You want to use it, not store it.
This is another in a big list of things developed for T2’s that they start putting T1’s on.