I thought high insulin and high glucose cause fat storage and weight gain and that the weight loss associated with Victoza was for the loss of appetite it induces. May be I am wrong?
Yes, I see that the prescription of Victoza in my case is weird. Everyone who commented on my post pointed out to that too. I will have to go back to my doc and revise the use of Victoza especially giving its side effects.
Actually, thinking about that what I wrote, I am not entirely happy with it myself. I can see it taking effect with very high sugar levels, and high insulin, which is a condition one step away from diabetic coma, so really is the option of last resort as it were. But it does not explain what may be happening in connection with this medication, which occurs at not particularluy high glucose levels. So something else is going on.
The timing of the injecion is not connected to eating or fasting. It is not dependant on any particular diet or nutrient. It does not need a glucose hit to start it off (as a sulfonyl med does) and it overrides the GLP-1 pathway forcing an insulin response regardless of glucose level. It is stated that hypos do not occur so the ketosis is not related to glucose (unlike dietary ketosis). So there may be some thing associated with insulin being pumped out willy nilly due to the GLP=1 clamp, but without there being food under digestion or triggering the normal GLP=1 enzyme or the lipase generated enzymes either. Maybe this combination of insulin with glucose already in the blood and not having the normal enzyme handshaking going on, then that is causing the fat burning. But then this status is actually a normal stage for a T2D with hyperinsulinenia, and we do not seem to get DKA from that condition. All I can think of is that there is some mechanism that both the SGLT-2 meds and the GLP-1 meds is upsetting that either stops the body getting rid of ketones or overrides the Krebs Cycle to force fat burning (as I said, weight loss appears to be more than just glycogen and seems to involve lipids too).
I think the thing that worries me is that a drug like Gliclazide (which I am using) also increases insulin output but is not associated with DKA like the others I mentioned above. But it is also limited in scope and passes out of the system in a matter of hours so any effect from it is transitory, The binding of the GLP-1 receptors is an override that I suspect has a longer half life, which is why the inections are weekly, so once in the body, it may be not be easy to control it. But the SGLT-2 meds are also daily pills and they can cause DKA, so still not explaining it. Dunno, its above my paygrade.
All I know is that I have had the experience of extended periods with glucose levels above what my meter can read (>32mmol/l) and I know my pancreas is still producing insulin . At the time I was maxed out on the Gliclazide, so thrashing my pancreas without DKA. It is not simply high insulin or high glucose or low carbs. But ketones and fruity breath are listed as common side effects of the gliptin meds. Its there for a reason since my gliclazide does not have this side effect, nor any causation of DKA (unless the pancreas output is faulty) but does list hypoland as a probable destination.