Beyond reducing fasting blood glucose levels, berberine lowers blood plasma triacylglycerol (stored fat) and free fatty acid levels, reduces levels of C-reactive protein (an important marker for chronic inflammation) and cholesterol, ultimately leading to improved peripheral insulin sensitivity and nutrient uptake.
Furthermore, berberine stimulates the up-regulation of the expression of the enzyme 5'-adenosine monophosphate-activated protein kinase (AMPK) [a key enzyme and "molecular master switch" that plays a critical role in cellular energy homeostasis], mitogen-activated protein kinase (MAPK), p38 MAPK (for insulin-independent glucose uptake), peroxisome proliferator-activated receptor alpha (PPARa), uncoupling protein-2 (UCP-2), as well as hepatic (liver) nuclear factor 4 alpha (HNF4a). The activation of AMPK leads to inhibition of fatty acid synthesis (production) and increased fatty-acid (beta) oxidation in the liver and adipocytes (fat cells), as well as the synthesis of cholesterol in the liver. Conversely, it down-regulates the expression of peroxisome proliferator-activated receptor gamma (PPARg), PPARg cofactors, as well as resistin. In other words, berberine beneficially modulates glucose and lipid metabolism via multiple molecular mechanisms.
One mechanism through which berberine induces its anti-hyperglycemic activity is by acting as a potent competitive inhibitor of the human protein tyrosine phosphatase 1B (h-PTB1B). PTB1B is a negative regulator (inhibitor) of insulin signaling (or signal transduction), so that PTB1B levels are high in insulin-dysfunctional states. In other words, PTB1B down-regulates insulin action and insulin sensitivity in skeletal muscle and fat cells. Consequently, by inhibiting h-PTB1B, berberine allows the restoration of cellular insulin sensitivity and reduces plasma glucose levels.
In terms of the inhibition of lipid expression, berberine accomplishes this by blocking adipogenesis (new-fat formation) in fat cells via inhibition of PPARg and C/ERB alpha, and by activating PPARa. Furthermore, still on inhibition of lipid metabolism, berberine reduces GLUT4 mRNA expression in fat cells and also reduces the expression of multiple lipogenic and adipogenic genes in adipocytes (fat cells).
(Bulk) P-Slin can handle larger carbohydrate loads, in the range of 60-120g, at standard doses, or somewhat higher at increased doses. It is incredibly effective before a carbohydrate-containing pre-workout meal, disposes glucose efficiently and delivers real "food pumps". If fat-loss is not the primary concern, and if carbohydrate consumption is more in the high range, (Bulk) P-Slin is unmatched. Anabolic Pump on the other hand lends itself to more versatility. In particular, it can be used as a powerful fat-loss tool (when carbohydrate consumption is limited to 30-35g per dose of Anabolic Pump), can be part of a fat-loss stack, or can be used in a standard everyday fashion during its cycle or in lean-bulk or controlled-bulking scenario with normal carbohydrate consumption of up to 60-70gr. Its beauty is its ability to stimulate glucose uptake in skeletal muscle cells, at the expense of fat cells, thanks to the molecular mechanisms I enumerated earlier. Anabolic Pump and (Bulk) P-Slin can also be stacked. In this case, (Bulk) P-Slin is used for the largest carbohydrate meal during the day, while Anabolic Pump can be used for two othe carbohydrate-containing meals. They can also be used before cheat meals.