No: Most of the research on Berberine - and to an extent Lagerstroemia - has reflected antilipogenic activity via PPAR-Gamma2, and not Alpha. However, AMPk does play a role in the upregulation of PPAR-Alpha in skeletal muscle in the context of oxidative energy demands in endurance training sessions; that is beside the point, though. I merely pointed out PPAR-Alpha, in order to point out the fallacy of your CPT-1 comment. AP predominantly mediates Gamma, which does not have transcriptional control over either malonyl-COA or the target enzyme CPT-1. In reality, most of the research concerning upregulated malonyl-CoA and subsequent lessened mRNA CPT-1 expression surrounded Alpha's activity in smooth muscle; the context is different.
My comments towards AMPk are vital to the discussion at hand, though; energy homeostasis, and by extension Anabolic Pump's MOA, cannot be fully understood without a concomitant understanding of AMPk mediated FA oxidation, glucose metabolism, protein synthesis, and so on. AMPk responds to extracellular fluctuations (AMP:ATP ratio) in order to meet intracellular demand for energy. It is especially responsible for the transferring between glycolytic and oxidative manners of energy expenditure during anaerobic exercise (see above comment). It directly controls the expression of GLUT4, and the processes of glycolysis and vasculogenesis, as well as mediating several other glucose uptake enzymes. It is highly responsible for the efficient storage and expenditure of glucose - hence my comments towards your 'excess glucose' storage comment.
Further, AMPk inactivates ACC, and upregulates levels of MCD (malonyl-CoA-decarboxylase) which as you know leads to increased levels of CPT-1 and subsequent mitochondrial FA oxidation. So, as I said earlier, CPT-1 is not an issue in this respect, and AP is - very efficiently so - antilipogenic. This is one of the primary mechanisms through which AP produces body composition changes: Ensuring the efficient transfer and storage of glucose, as well as increasing the cell's oxidative capacity. The risk of FA 'restorage' and subsequent lipogenesis/lipid hypertrophy is therefore reduced, and AMPk by its nature prevents plasma triglyceride, and lipid synthesis.
I appreciate your healthy skepticism, but I also appreciate my reps being allowed to conduct their activities without overzealous posters harassing them with condescending tones and questions they do not fully understand. Your confrontational attitude isn't necessary, and I hope in further USP Labs related threads you participate in, you are much more cordial.