To be honest, up until now I have only seen the name in some threads. I just read the description of it in the AM store.
Now keep in mind that this is a theoretical only discussion based on the product claims. It sounds problematic.
Insulin is an energy management hormone for which lowering blood glucose is only a function. Insulin allows your body to use the energy that you eat. When circulating macro nutrients are above baseline, insulin will move the surplus into one of the 'storage receptacles' (ie. glycogen in muslces and liver or body fat). The body, probably for survival reasons, does not discard energy.
According to the description, Anabolic Pump sensitizes muscles to insulin and desensitizes fat cells to it. However, glycogen is still a relatively small receptacle compared to the nearly limitless capacity of bodyfat. If your surplus energy exceeds the capacity of glycogen storage then where does it go if the Anabolic Pump blocks it from being moved to body fat? Nowhere, back to square one with a surplus of blood glucose and FFAs.
Now I seriously doubt that Anabolic Pump modifies sensitivities to that extent but it serves for the sake of the argument. While shifting one's genetic program towards leaner bodycomp may be a high priority for non diabetic bodybuilders, doing so at the expense of reducing insulin sensitivity on our largest energy storage receptacle proably isnt the best approach for diabetics.
Hope that makes sense.
You're right insofar as the energy expenditure problematic; if an NIDDM patient is to dose the product, and not exceed the necessary energy expenditure, does he/she remain hyperglycemic? The answer, for the most part, is no.
This is happening by way of three mechanisms. One you mentioned above being the increased permeability to glycogen of muscle cells, and the second is by way of AMP-K modulation[1,2]. AMP-K is a prominent gene in relation to energy expenditure, and is paramount to inhibiting lipogenesis. Berberine, a constituent of AP, is found to due the stated, and this is part of its antihyperglycemic effect. [2]
It is interesting you mention the weariness for a Diabetic, because Berberine and Tannins are both extremely promising alternative treatments for NIDDM; especially as it pertains to presenting a viable alternative to synthetic alpha-glucosidase inhibitors. This A-G inhibition was the third MOA I mentioned which imparts Berberine with anti-hyperglycemic capabilities [3]. By inhibiting saccharide release at the gastrointestinal level, this ensures a stable release of blood sugar, and subsequent release of Insulin; also, this addresses the excess blood sugar you mentioned above.
With GLUT4 translocation shown to be double that of control groups in myocytes, AMPK expression upregulated in adipocytes, lipogenesis controlled, and anti-glucosidase activity in the intestine, Berberine creates an environment which is extremely conducive to not only battling NIDDM, but the symptoms of high blood pressure and obesity which are corollary with this condition.
In all of the human NIDDM models I have seen Berberine a) lowered cholesterol b) lowered blood glucose and c) addressed obesity.
And that's not even talking about the Tannins complex in AP! (it's also shown to increase GLUT4 translocation and inhibit adipocyte differentiation).
[1] Berberine-stimulated glucose uptake in L6 myotubes involves both AMPK and p38 MAPK. Zhe Cheng, Tao Pang, Min Gu, An-Hui Gao, Chuan-Ming Xie, Jia Li, Fa-Jun Nan.
[2] Berberine, a Natural Plant Product, Activates AMP-Activated Protein Kinase With Beneficial Metabolic Effects in Diabetic and Insulin-Resistant States. Yun S Lee, Woo S Kim, Kang H Kim, Myung J Yoon.
[3] Berberine Has Some Anti-alpha Glucosidase Activity. Pan G, Huang Z, Wang G, et al,