About the AP/berb thing, I was just posting to show proof that berb works differently than how USP says AP works.
High protein diet is questionable. The whole AMPK activation reducing protein synthesis thing is transient; for the relatively little time that AMPK is activated initially, protein synthesis is stopped as AMPK signals an energy deficit in muscle; protein synthesis occurs to repair muscle, but is I believe a secondary action to replenishing ATP stores.
A high protein diet is rich in all the amino acids, and suffers from delayed absorption. I suggested leucine because of its quick absorption through the gastrointestinal tract and quick effect on protein synthesis. Seeing as we are worried about a relatively small time in relation to a 24 hour period, leucine spiking (or BCAAs) could serve to counteract the delay in protein synthesis.
Then again, I'm not sure if forcing protein synthesis concurrent with AMPK activation is possible, or even if it would mitigate the effects of the berberine.
I have seen research showing that chronic AMPK activation ends up with above normal levels of muscle glycogen in the long run without any problems in muscle size; leucine might only be an unecessary precaution.
Regarding ALA:
Entrez PubMed
The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM).
Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement.
Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.
I post this because of the italicized and bolded comments; ALA exerts its effects through insulin-mediated mechanisms, which differs from berberine's effects. So in theory yes, they could both be used. However, ALA definately exerts its effects in adipocyte as well as skeletal muscle; berberine seems to be somewhat independent of insulin.