So I’ve encountered some interesting papers which discuss the likely MOA of berberine and it was quite surprising to me because the MOA that these two papers point to is very different to what has been discussed in regards to how berberine works. It also raises a question for me in regards to if this ingredient is all that great of an ingredient to use for healthy individuals whom are aiming for performance rather than a medical need to lower their blood glucose levels and improve insulin sensitivity but metformin is not an option.
Now, we know that metformin likely has AMPK effects as well as mitochondrial effects. It is also readily bioavailabile as the majority of it does get absorbed through digestion. There are also unknown mechanisms which are not understood about metformin as well but the key here that I want to point out is that it is readily absorbed through digestion and it has been demonstrated that it has its effects directly at the cellular level as the drug does make it into cells to impart its effects.
Berberine, the effects of berberine on the measures of blood glucose and insulin levels are positive and it has of course been positively compared to metformin but the mechanism of action is assumed that it has similar MOAs as metformin (at least when one compares berberine freely and often to metformin, that is the implication being insinuated). Now in Berberine acutely inhibits the digestion of maltose in the intestine Zeng-Qiang Li et al. J Ethnopharmacol. 2012 and Inhibitory action of berberine on glucose absorption Guo-yu Pan et al. Yao Xue Xue Bao. 2003, it is suggested that the likely MOA of berberine is it’s inhibition of alpha-glucosidase. What does this imply? This would suggest that berberine inhibits the break down of starches to simple sugars. This MOA are also noted as likely major MOA for glucose and insulin controlling effects of berberine in the paper Berberine in Cardiovascular and Metabolic Diseases: From Mechanisms to Therapeutics Xiaojun Feng, Antoni Sureda, [...], and Ai-Zong Shen. So the question is this, as I’m not smart enough to answer it nor do I have any sort of research background to do so, is berberine actually all that great of an ingredient to use outside of a treatment for type 2 diabetics. Considering our purpose is wanting nutrient partitioning effects when using GDAs not nutrient malabsorption (effectively from what I understand, inhibiting alpha-glucosidase is effectively malabsorption of starches?). The major MOA here would suggest that the dominant effects it has in regards to glucose and insulin control has to do with it’s effects in the small intestine rather than at a cellular level like how metformin works. Both results in positive changes in markers but the two appear to do so by very different mechanisms where the one for berberine appears questionable for our purposes.
Now, we know that metformin likely has AMPK effects as well as mitochondrial effects. It is also readily bioavailabile as the majority of it does get absorbed through digestion. There are also unknown mechanisms which are not understood about metformin as well but the key here that I want to point out is that it is readily absorbed through digestion and it has been demonstrated that it has its effects directly at the cellular level as the drug does make it into cells to impart its effects.
Berberine, the effects of berberine on the measures of blood glucose and insulin levels are positive and it has of course been positively compared to metformin but the mechanism of action is assumed that it has similar MOAs as metformin (at least when one compares berberine freely and often to metformin, that is the implication being insinuated). Now in Berberine acutely inhibits the digestion of maltose in the intestine Zeng-Qiang Li et al. J Ethnopharmacol. 2012 and Inhibitory action of berberine on glucose absorption Guo-yu Pan et al. Yao Xue Xue Bao. 2003, it is suggested that the likely MOA of berberine is it’s inhibition of alpha-glucosidase. What does this imply? This would suggest that berberine inhibits the break down of starches to simple sugars. This MOA are also noted as likely major MOA for glucose and insulin controlling effects of berberine in the paper Berberine in Cardiovascular and Metabolic Diseases: From Mechanisms to Therapeutics Xiaojun Feng, Antoni Sureda, [...], and Ai-Zong Shen. So the question is this, as I’m not smart enough to answer it nor do I have any sort of research background to do so, is berberine actually all that great of an ingredient to use outside of a treatment for type 2 diabetics. Considering our purpose is wanting nutrient partitioning effects when using GDAs not nutrient malabsorption (effectively from what I understand, inhibiting alpha-glucosidase is effectively malabsorption of starches?). The major MOA here would suggest that the dominant effects it has in regards to glucose and insulin control has to do with it’s effects in the small intestine rather than at a cellular level like how metformin works. Both results in positive changes in markers but the two appear to do so by very different mechanisms where the one for berberine appears questionable for our purposes.