Hi Marit,

T2D is based on the conjonction of genetics background and environment. patients with complete remission certainly followed critical change in their way of life (more sports, less carbohydrates and fatty acids, weight loss...). but still the genetics is here and if they don't follow their diet there is no reason for T2D to return. See lot of sportsmen that abandon their lifestyle other 40 and become T2D.

fred

Sorry Marit,

my 2 last sentences show errors, here are the corrections:

there is no reason for T2D not to return. See lot of sportsmen that abandon their lifestyle over 40 and become T2D.

fred

Thank you Frederic, but my question was not really answered. I'm after the definition of remission used by the researchers working with the Virta treatment.

Hi Marit,

I guess you're talking about this solution (https://www.virtahealth.com/thevirtatreatment), and they base the remission only on approving blood sugar (Hba1C) and weight loss. But it's not magic, as soon as you stop their treatment (which is expensive), you'll loose these benefits and become again T2D.

fred

Frederic Lepretre Thanks, that was helpful. Now I found their definition of reversal: " Note that % reversal is defined as the % of patients with HbA1c less than 6.5% who are taking no glycemic control medications or only metformin" Not impressed! I find the term "reversal" should not be used in this contexts. "Slight improvement" seems to be more accurate..

Hi Marit,

I agree, reversal is a strong word hardly difficult to maintain in genetic diseases...

all the best

fred

Hi Marit,

I found some research you need to follow, especially works done by R Taylor (https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)33102-1/fulltext).

all the best

fred

Frederic Lepretre; Thanks a lot! Remission here is defined as: "HbA1c less than 6·5% (

agree completely

fred

Hi Marit and all scientists in the field of type 2 diabetes,

Attached you will find an answer on your question.

Rob

Rob Weijers - Thank you, that was a very interesting angle. Cell membranes is a forgotten topic in diet-related conditions, in my opinion. Is this genetic disposition (that causes re-enter of H+ throught the UCPs) common in persons developing diabetes? And - wouldn't an increase in cell temperature rather increase the membrane flexibility/fluidity (or maybe increased flexibility does not equal increased fluidity)? Totally agree with the suggestion for a new title.

Marit

Hi Marit,

With regard to your first question, I propose that this genetic disposition is almost certainly common in persons developing type 2 diabetes. My answer to the second question is that an increase in cell temperature the UI reduces, which reduces the functionality of all Class I glucose transporters due to an increased lateral contraction of the transporter protein. A smaller cross-sectional pore surface reduces the glucose transport velocity, with all the implications that this entails.

Rob

Rob Weijers Thank you, that makes sense. So would this mechanism be instead of or in addition to the hypothesis that inflammation causes activation of stress kinases, which reduces senitivity to insulin? (By phosphorylating insulin receptors on serin/treonin residues, making the receptor less likely to auto-phosphorylate on tyrosin)

Complete remission of the type-2 will be possible, but certainly at what stages, the interventions are done. As rightly pointed out if we can up-regulate the sensitivity of all insulin receptors (GLUT4) I think surely it will revert the condition. Further subject may also able to take normal balance diet, rather carbohydrate rich diet, which may again trigger the pathogenesis nexus. But if we are expecting the revert after a chronic type of DM-2, where the exhausted pancreatic beta cell will be unable to secrete insulin (as they are damaged) and hence could lead the all complicated consequences along inflammatory responses making remission impossible.