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Modern clinical use and published in vivo, in vitro, and animal research studies demonstrate that the berberine metabolite dihydroberberine (DHB) is more bioavailable than berberine and offers enhanced support for healthy blood glucose metabolism.*1-5 Although the mechanisms underlying the beneficial effects of berberine are not entirely clear, it is hypothesized that the modulation of gut microbes may be one mechanism by which berberine affects blood glucose metabolism.6 Results from animal and in vitro studies suggest that berberine moderates glucose and lipid metabolism through a multi-pathway mechanism, including the adenosine monophosphateactivated protein kinase (AMPK), c-Jun N-terminal kinase (JNK), and peroxisome proliferator-activated receptor (PPAR)-alpha pathways.2,7 Separate research on AMPK reports activating the AMPK pathway stimulates glucose uptake and fat oxidation while suppressing lipogenesis and gluconeogenesis.8 Berberine is also believed to be involved in the regulation of pancreatic beta cell function, and it has been observed to inhibit the expression of disaccharidases in the duodenum, resulting in less glucose formation from carbohydrate digestion.*9 Increasing evidence indicates that gut microbiota are also crucial mediators that regulate berberines pharmacokinetic and biological effects

It is commonly studied in laboratory environments for its potential role in metabolic and biochemical research, particularly in pathways related to lipid metabolism and energy regulation