20 replies to this topic

[lumia]

A lot has been discussed about berberine's AMPK activation effects and antibiotic effects, but it (as the purified chemical) is first used as an oral antibacterial for GI infections, and even up to this day some researcher still do berberine research on its antibacterial effects:

 

BMC Complement Altern Med. 2014; 14: 89.
Role of berberine in anti-bacterial as a high-affinity LPS antagonist binding to TLR4/MD-2 receptor
Ming Chu, Ran Ding, Zheng-yun Chu, Ming-bo Zhang, Xiao-yan Liu, Shao-hua Xie, Yan-jun Zhai, and Yue-dan Wang

Background
Berberine is an isoquinoline alkaloid mainly extracted from Rhizoma Coptidis and has been shown to possess a potent inhibitory activity against bacterial. However, the role of berberine in anti-bacterial action has not been extensively studied.

Methods
The animal model was established to investigate the effects of berberine on bacterial and LPS infection. Docking analysis, Molecular dynamics simulations and Real-time RT-PCR analysis was adopted to investigate the molecular mechanism.

Results
Treatment with 40 mg/kg berberine significantly increased the survival rate of mice challenged with Salmonella typhimurium (LT2), but berberine show no effects in bacteriostasis. Further study indicated that treatment with 0.20 g/kg berberine markedly increased the survival rate of mice challenged with 2 EU/ml bacterial endotoxin (LPS) and postpone the death time of the dead mice. Moreover, pretreatment with 0.05 g/kg berberine significantly lower the increasing temperature of rabbits challenged with LPS. The studies of molecular mechanism demonstrated that Berberine was able to bind to the TLR4/MD-2 receptor, and presented higher affinity in comparison with LPS. Furthermore, berberine could significantly suppressed the increasing expression of NF-κB, IL-6, TNFα, and IFNβ in the RAW264.7 challenged with LPS.

Conclusion
Berberine can act as a LPS antagonist and block the LPS/TLR4 signaling from the sourse, resulting in the anti-bacterial action.

→ source (external link)

 

Which makes me wonder whether berberine will modify gut flora, and more than one papers on PubMed say yes:

 

Sci Rep. 2015 Sep 23;5:14405.

Modulation of gut microbiota by berberine and metformin during the treatment of high-fat diet-induced obesity in rats.

Zhang X, Zhao Y, Xu J, Xue Z, Zhang M, Pang X, Zhang X, Zhao L.

Accumulating evidence suggests that the gut microbiota is an important factor in mediating the development of obesity-related metabolic disorders, including type 2 diabetes. Metformin and berberine, two clinically effective drugs for treating diabetes, have recently been shown to exert their actions through modulating the gut microbiota. In this study, we demonstrated that metformin and berberine similarly shifted the overall structure of the gut microbiota in rats. Both drugs showed reverting effects on the high-fat diet-induced structural changes of gut microbiota. The diversity of gut microbiota was significantly reduced by both berberine- and metformin-treatments. Nearest shrunken centroids analysis identified 134 operational taxonomic units (OTUs) responding to the treatments, which showed close associations with the changes of obese phenotypes. Sixty out of the 134 OTUs were decreased by both drugs, while those belonging to putative short-chain fatty acids (SCFA)-producing bacteria, including Allobaculum, Bacteriodes, Blautia, Butyricoccus, and Phascolarctobacterium, were markedly increased by both berberine and, to a lesser extent, metformin. Taken together, our findings suggest that berberine and metformin showed similarity in modulating the gut microbiota, including the enrichment of SCFA-producing bacteria and reduction of microbial diversity, which may contribute to their beneficial effects to the host.

→ source (external link)

 

Arch Iran Med. 2016 Mar;19(3):197-203. doi: 0161903/AIM.008.

Modulation of Gut Microbiota by Berberine Improves Steatohepatitis in High-Fat Diet-Fed BALB/C Mice.

Cao Y, Pan Q, Cai W, Shen F, Chen GY, Xu LM, Fan JG.

BACKGROUND: Dysbiosis of the gut microbiota underlies non-alcoholic steatohepatitis (NASH). Ingredient of Chinese herbal medicine, berberine, has been proved to regulate the gut microbiota without systemic side effects. Therefore, we explored its effects on NASH induced by high-fat diet (HFD).

METHODS: BALB/c mice were randomized into three groups, including: control, model, and berberine treatment. With the exception of the control group with the standard diet, the model, and the treatment groups were treated by HFD. Mice from treatment group were further subjected to berberine (200 mg/kg/d) gavage since the 5th week. At the end of the 13th week, gut bacteria, liver endotoxin receptor, and inflammation cytokines were assessed by real-time PCR. NASH and its predisposing factors were evaluated biochemically and pathologically.

RESULTS: Compared to their decreases in the model group, berberine administration restored the relative level of Bifidobacteria (2.16 ± 0.63 vs. 0.50 ± 0.08, P < 0.01) and the ratio of Bacteroidetes/ Firmicutes (0.76 ± 0.26 vs. 0.39 ± 0.11, P < 0.01), respectively, in the treatment groups. Microbiota restoration led to significant reductions in body weight, serum levels of lipids, glucose, insulin, and homeostasis model assessment of insulin resistance. Improvements were also observed in the serum transaminase activity and nonalcoholic fatty liver disease activity score, which demonstrated the attenuation of NASH. Mechanically, expression levels of CD14, IL-1, IL-6 and TNF-α were statistically down-regulated (treatment group vs model group, P < 0.01).

CONCLUSIONS: Berberine alleviates NASH and its predisposing factors. Normalization of gut microbiota might underlie its effect.

→ source (external link)

 

While both papers sees the change in microbiota composition following berberine administration as positive, I'm not completely sure if I should necessarily believe in their opinion at this stage. Still, I sort-of think berberine is probably a relative safe thing to take, unlike Jiaogulan (gynostemma), which has known insulin-releasing effects...

 

I wonder whether spacing out berberine and a probiotic should resolve any conflict caused?

[normalizing]

i read a lot of papers on berberine being an antidepressant but im losing hope in all studies on this because i was dosing quite high on it for few days with absolutely zero effect except severe yellow stools which might make some worry if one didnt know berberine is a serious yellow colorant

[GoingPrimal]

Lumia, could you expand on the insulin-releasing effects of gynostemma? I would be hesitant to call an adaptogenic herb with hundreds of years of safe use as relatively unsafe, especially with so many positive studies and anecdotes behind it, although it very well may be that I'm simply misunderstanding you.

Edited by GoingPrimal, 27 March 2016 - 08:49 PM.

[lumia]

Lumia, could you expand on the insulin-releasing effects of gynostemma? I would be hesitant to call an adaptogenic herb with hundreds of years of safe use as relatively unsafe, especially with so many positive studies and anecdotes behind it, although it very well may be that I'm simply misunderstanding you.

 

I read at least one paper that shows gynostemma extract is insulin releasing in rats:

 

Evid Based Complement Alternat Med. 2015;2015:120572. doi: 10.1155/2015/120572. Epub 2015 Jun 23.
Evaluation of Antidiabetic Effects of the Traditional Medicinal Plant Gynostemma pentaphyllum and the Possible Mechanisms of Insulin Release.
Lokman EF, Gu HF, Wan Mohamud WN, Östenson CG.

Aims. To evaluate the antidiabetic effects of Gynostemma pentaphyllum (GP) in Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, and to investigate the mechanisms of insulin release. Methods. Oral glucose tolerance test was performed and plasma insulin levels were measured.

Results. An oral treatment with GP (0.3 g/kg of body weight daily) for two weeks in GK rats improved glucose tolerance versus placebo group (P < 0.01). Plasma insulin levels were significantly increased in the GP-treated group. The insulin release from GP-treated GK rats was 1.9-fold higher as compared to the control group (P < 0.001). GP stimulated insulin release in isolated GK rat islets at high glucose. Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response to GP. Furthermore, the protein kinase A (PKA) inhibitor H89 decreased the insulin response to GP (P < 0.05). In addition, GP-induced insulin secretion was decreased after preincubation of GK islets with pertussis toxin to inhibit exocytotic Ge proteins (P < 0.05).

Conclusion. The antidiabetic effect of GP is associated with the stimulation of insulin release from the islets. GP-induced insulin release is partly mediated via K-ATP and L-type Ca(2+) channels, the PKA system and also dependent on pertussis toxin sensitive Ge-protein.

→ source (external link)

[normalizing]

that doesnt sound good does it

[GoingPrimal]

 

Lumia, could you expand on the insulin-releasing effects of gynostemma? I would be hesitant to call an adaptogenic herb with hundreds of years of safe use as relatively unsafe, especially with so many positive studies and anecdotes behind it, although it very well may be that I'm simply misunderstanding you.

 

I read at least one paper that shows gynostemma extract is insulin releasing in rats:

 

Evid Based Complement Alternat Med. 2015;2015:120572. doi: 10.1155/2015/120572. Epub 2015 Jun 23.
Evaluation of Antidiabetic Effects of the Traditional Medicinal Plant Gynostemma pentaphyllum and the Possible Mechanisms of Insulin Release.
Lokman EF, Gu HF, Wan Mohamud WN, Östenson CG.

Aims. To evaluate the antidiabetic effects of Gynostemma pentaphyllum (GP) in Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, and to investigate the mechanisms of insulin release. Methods. Oral glucose tolerance test was performed and plasma insulin levels were measured.

Results. An oral treatment with GP (0.3 g/kg of body weight daily) for two weeks in GK rats improved glucose tolerance versus placebo group (P < 0.01). Plasma insulin levels were significantly increased in the GP-treated group. The insulin release from GP-treated GK rats was 1.9-fold higher as compared to the control group (P < 0.001). GP stimulated insulin release in isolated GK rat islets at high glucose. Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response to GP. Furthermore, the protein kinase A (PKA) inhibitor H89 decreased the insulin response to GP (P < 0.05). In addition, GP-induced insulin secretion was decreased after preincubation of GK islets with pertussis toxin to inhibit exocytotic Ge proteins (P < 0.05).

Conclusion. The antidiabetic effect of GP is associated with the stimulation of insulin release from the islets. GP-induced insulin release is partly mediated via K-ATP and L-type Ca(2+) channels, the PKA system and also dependent on pertussis toxin sensitive Ge-protein.

→ source (external link)

 

 

It's definitely an interesting find, but again I think it points towards gynostemma's adaptogenic properties. The type of rat they used for the study (Goto-Kakizaki rats), are genetically engineered to have Type II diabetes, which in many cases means both insulin resistance and a lack of insulin release in response to glucose. Seeing as gynostemma-treated rats released more insulin in response to glucose than did non-treated rats, this seems (to me at least) to be a beneficial thing. 

 

I for one would love to see if there is an insulin-releasing response in healthy humans, never mind rats that have been genetically predisposed to having type II diabetes.

[maxwatt]

Berberine works better combined with baicalin, best with a ratio 2:1 Berberine to baicalin.   These are also two of the major components of traditional Chines medicine, "Huan Liang Jie du Tang".

[Psilociraptor1]

I don't know why the author suggested a reduction in diversity was a positive effect. Diversity is one of the only consistent factors of a healthy microbiome we currently know of. That said I made this account mostly to reply to this... While I can't give anything other than personal experience, my impressions are that berberine can utterly destroy your microbiome if you're not careful with it. I've been suffering autoimmune issues for a while now and was mostly stable after months of strict diet regulations. I got a stool test showing an insane amount of E. coli and decided I'd try to knock it back with berberine. I kept titrating the dose up until the die off effects maxed and subsided. But as soon as I stopped taking it it came back with a vengeance. It has been months now and I'm still recovering from that mistake... Maybe. I've noticed some dark spots im paranoid are melanomas now. Maybe they are maybe they're not. Either way it's one of the few things I seriously regret doing. Berberine is just as dangerous as any other broad spectrum antimicrobial.

[YOLF]

I've definitely noted the need for probiotics after using berberine, but it does work excellent for all sorts of infections when used at the first sign. I wouldn't think of using it without the widest spectrum probiotic on the market though. I think I take a total of 20 different organisms post berberine and there is still some microbiome recovery involved. Barberry Bark isn't much better, but it's a little bit more gentle, though perhaps also less effective.

[lumia]

I've definitely noted the need for probiotics after using berberine, but it does work excellent for all sorts of infections when used at the first sign. I wouldn't think of using it without the widest spectrum probiotic on the market though. I think I take a total of 20 different organisms post berberine and there is still some microbiome recovery involved. Barberry Bark isn't much better, but it's a little bit more gentle, though perhaps also less effective.

 

The problem is, it seems many people are taking it long term for AMPK/ diabetes, so there's not much "after" you can recover your microbiome. But is taking a wide spectrum probiotic a good idea while on berberine?

[YOLF]

I think it's a matter of dosing... most probiotics sold in stores don't have alot of CFUs in them, but other brands will have 1000s of times more. So it's a dosing issue in my experience. Retail probiotics are also a bit weak in terms of the numbers of unique organisms. Usually 3-4 tops if even 1 or 2. I take 20+ Taken with an antibiotic you do get the benefit of all the things that the dying probiotics leave behind. Lots of enzymes and such.

[Psilociraptor1]

So I should retract my earlier experience. Recent leads suggest most of my symptoms are most likely Lyme disease which complicates matters. Not to say berberine should be used indescriminately, but I think my reaction was quite dramatic for reasons not necessarily related to the gut microbiome

[Logic]

...Indeed, the gut barrier-protecting effects of berberine have been reported in animal models challenged with pro-inflammatory cytokines or LPS [42], [50], the mechanisms of which have been suggested to be the promotion of proglucagon mRNA expression and L cell proliferation in the intestine [27], [28]. Our findings suggest that this gut barrier-protecting function of berberine is mediated by elevated levels of SCFAs produced by selectively enriched SCFA producers in the gut...

http://journals.plos...al.pone.0042529

 

But SCFAs/Acetate make you fat...
http://www.longecity...ndpost&p=777850

http://www.longecity...ndpost&p=777864

 

[gamesguru]

the berberine would be really annoying when you're trying to maintain populations of Lactobacillus rhamnosus, for GABA, and Lactobacillus reuteri, for testosterone.

Gynostemma pentaphyllum Tea Improves Insulin Sensitivity in Type 2 Diabetic Patients
V. T. T. Huyen,1,2,3 D. V. Phan,2 P. Thang,3 N. K. Hoa,4 and C. G. Östenson1 (2013)

Aims. To evaluate the effect of the traditional Vietnamese herb Gynostemma pentaphyllum tea on insulin sensitivity in drug-naïve type 2 diabetic patients. Methods. Patients received GP or placebo tea 6 g daily for four weeks and vice versa with a 2-week wash-out period. At the end of each period, a somatostatin-insulin-glucose infusion test (SIGIT) was performed to evaluate the insulin sensitivity. Fasting plasma glucose (FPG), , and oral glucose tolerance tests and insulin levels were measured before, during, and after the treatment. Results. FPG and steady-state plasma glucose (SIGIT mean) were lower after GP treatment compared to placebo treatment ( ). The levels of FPG in the control group were slightly reduced to versus  mmol/L in GP group ( ), and the effect on FPG was reversed after exchanging treatments. The glycometabolic improvements were achieved without any major change of circulating insulin levels. There were no changes in lipids, body measurements, blood pressure, and no reported hypoglycemias or acute adverse effects regarding kidney and liver parameters. Conclusion. The results of this study suggested that the GP tea exerted antidiabetic effect by improving insulin sensitivity.

 

Supplemental Naringenin Prevents Intestinal Barrier Defects and Inflammation in Colitic Mice1,2,3
Tomoyo Azuma4,6, Mizuki Shigeshiro4,6, Michiyo Kodama5, Soichi Tanabe4, and Takuya Suzuki4 (2013)

Intestinal barrier defects are involved in the pathogenesis of inflammatory bowel disease. The present study investigated the ameliorative effects of naringenin, a citrus polyphenol, on intestinal tight junction (TJ) barrier defects and inflammation in a murine model of colitis. In Expt. 1, using a 2 × 2 fractional design, the mice were administered water or 2% dextran sulfate sodium (DSS) in combination with feeding control or naringenin-containing diets for 9 d (severe disease stage). DSS administration caused severe colon damage and inflammation, as indicated by body weight loss, increased clinical sores, colon shortening, and gene expressions of inflammatory cytokines [interferon-γ, interleukin (IL)-6, macrophage inflammatory protein-2, and IL-17A). DSS administration also impaired TJ barrier integrity in the colon, as indicated by increased colon permeability and plasma LPS-binding protein levels, resulting from the impaired colonic expression of TJ proteins, occludin, junctional adhesion molecule-A, and claudin-3. Supplemental feeding with naringenin totally or partially attenuated these symptoms, suggesting that naringenin ameliorates the DSS-induced colitis at least partially through protection of the TJ barrier. In Expt. 2, analyses were performed at different disease stages (d 3, 6, and 9) to more widely examine the ameliorative role of naringenin on the initiation and development of colitis. DSS administration moderately induced colon shortening at d 3 and 6 and increased the disease activity index (DAI) and inflammatory cytokine (IL-6 and IL-17A) expression without any significant increases in colonic permeability. Feeding naringenin attenuated the increased DAI and colon shortening and tended to suppress the increased cytokine expression. These findings suggest that the presence of an additional mechanism underlying the naringenin-mediated, anticolitic effect along with barrier protection.

 

ginseng is another one with interesting metabolism, depending on gut flora.

Edited by gamesguru, 09 June 2016 - 05:28 PM.

[joelcairo]

...Indeed, the gut barrier-protecting effects of berberine have been reported in animal models challenged with pro-inflammatory cytokines or LPS [42], [50], the mechanisms of which have been suggested to be the promotion of proglucagon mRNA expression and L cell proliferation in the intestine [27], [28]. Our findings suggest that this gut barrier-protecting function of berberine is mediated by elevated levels of SCFAs produced by selectively enriched SCFA producers in the gut...

http://journals.plos...al.pone.0042529

 

But SCFAs/Acetate make you fat...
http://www.longecity...ndpost&p=777850

http://www.longecity...ndpost&p=777864

 

I didn't go into all the studies mentioned in the other threads, but the first article you posted clearly states that berberine lowered obesity, at least partly through enhancing SCFA-producing bacteria.

 

Overall I don't see anything in any of the studies posted in this thread to make me worry about berberine. It doesn't slash and burn its way through the microbiome; it simply seems to change the gut homeostasis in favor of bacteria which are less inflammatory and more healthful, at least in animals.

[normalizing]

it is an antibiotic just take it with a grain of salt. not sure as of yet which bacteria kills exactly and how and if prolonged use is really a good idea most is short term few reports etc. but from personal experience that stuff gave me severe diarrhea and yellow piss water profusely fussing out was nasty. i think it definitely affects good bacteria because of gastrointestinal disturbances week later

[gamesguru]

there shouldn't be issues with bacteria resistance or tolerance, because berberine reversibly inhibits both DNA topoisomerase I and II. most inhibitors are irreversible, and berberine's reversibility seems to throw resistant strains for a loop. (see full study, and bottom text)

i agree it probably hurts good bacteria. it might also not be ideal for hypokalemia

[Inhibitory effect of berberine on potassium channels in guinea pig ventricular myocytes].
Hua Z1, Wang XL. (2004)

The effects of berberine on potassium channel subtypes were investigated by using patch-clamp whole cell recording techniques. Berberine is known to be effective in lowering blood glucose and ameliorating arrhythmia. Our results indicate that, berberine can prolong action potential duration (APD), decrease IK1 and outward Itail, but showed no effect on IK. In addition, berberine was also shown to antagonize cromakalim (BRL-34915) induced inhibition of APD and the increase of KATP. These suggest that berberine can inhibit voltage- dependent and ATP-sensitive potassium channels. It appears that the mechanisms of antiarrhythmic and antidiabetic action of berberine might be due to its potassium channel blocking effects.

 

Bacterial topoisomerases, anti-topoisomerases, and anti-topoisomerase resistance.
Hooper DC1. (1998)

Topoisomerases are ubiquitous enzymes necessary for controlling the interlinking and twisting of DNA molecules. Among the four topoisomerases identified in eubacteria, two, DNA gyrase and topoisomerase IV have been exploited by nature and the pharmaceutical industry as antibacterial targets. Natural products that are inhibitors of one or both of these topoisomerases include the coumarin and cyclothialidine classes, which interfere with adenosine triphosphate hydrolysis, cinodine, flavones, and terpenoid derivatives. The plasmid-encoded bacterial peptides micron B17 and CcdB also inhibit DNA gyrase. The quinolones, a synthetic class of antibacterials that act on both DNA gyrase and topoisomerase IV have had the broadest clinical applications, however. Quinolone congeners differ in their relative potencies for DNA gyrase and topoisomerase IV Studies of an expanding set of resistant mutant enzymes and the crystal structure of the homologous enzyme in yeast have contributed to our understanding of interactions of these drugs with topoisomerase-DNA complexes and the ways in which mutations effect resistance.

Edited by gamesguru, 10 June 2016 - 01:18 AM.

[lumia]

 

 

Lumia, could you expand on the insulin-releasing effects of gynostemma? I would be hesitant to call an adaptogenic herb with hundreds of years of safe use as relatively unsafe, especially with so many positive studies and anecdotes behind it, although it very well may be that I'm simply misunderstanding you.

 

I read at least one paper that shows gynostemma extract is insulin releasing in rats:

 

Evid Based Complement Alternat Med. 2015;2015:120572. doi: 10.1155/2015/120572. Epub 2015 Jun 23.
Evaluation of Antidiabetic Effects of the Traditional Medicinal Plant Gynostemma pentaphyllum and the Possible Mechanisms of Insulin Release.
Lokman EF, Gu HF, Wan Mohamud WN, Östenson CG.

Aims. To evaluate the antidiabetic effects of Gynostemma pentaphyllum (GP) in Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, and to investigate the mechanisms of insulin release. Methods. Oral glucose tolerance test was performed and plasma insulin levels were measured.

Results. An oral treatment with GP (0.3 g/kg of body weight daily) for two weeks in GK rats improved glucose tolerance versus placebo group (P < 0.01). Plasma insulin levels were significantly increased in the GP-treated group. The insulin release from GP-treated GK rats was 1.9-fold higher as compared to the control group (P < 0.001). GP stimulated insulin release in isolated GK rat islets at high glucose. Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response to GP. Furthermore, the protein kinase A (PKA) inhibitor H89 decreased the insulin response to GP (P < 0.05). In addition, GP-induced insulin secretion was decreased after preincubation of GK islets with pertussis toxin to inhibit exocytotic Ge proteins (P < 0.05).

Conclusion. The antidiabetic effect of GP is associated with the stimulation of insulin release from the islets. GP-induced insulin release is partly mediated via K-ATP and L-type Ca(2+) channels, the PKA system and also dependent on pertussis toxin sensitive Ge-protein.

→ source (external link)

 

 

It's definitely an interesting find, but again I think it points towards gynostemma's adaptogenic properties. The type of rat they used for the study (Goto-Kakizaki rats), are genetically engineered to have Type II diabetes, which in many cases means both insulin resistance and a lack of insulin release in response to glucose. Seeing as gynostemma-treated rats released more insulin in response to glucose than did non-treated rats, this seems (to me at least) to be a beneficial thing. 

 

I for one would love to see if there is an insulin-releasing response in healthy humans, never mind rats that have been genetically predisposed to having type II diabetes.

 

 

I found one study on humans with Type II Diabetes; there is a very mild increase in fast insulin levels after 6 weeks of gynostemma tea (from ~124 pmol/L to ~131 pmol/L), but it's hardly statistically significant due to very large intra-group variation. Other

J Nutr Metab. 2013;2013:765383. doi: 10.1155/2013/765383. Epub 2013 Jan 31.

Gynostemma pentaphyllum Tea Improves Insulin Sensitivity in Type 2 Diabetic Patients.

Huyen VT¹, Phan DV, Thang P, Hoa NK, Ostenson CG.

 

Aims. To evaluate the effect of the traditional Vietnamese herb Gynostemma pentaphyllum tea on insulin sensitivity in drug-naïve type 2 diabetic patients.

Methods. Patients received GP or placebo tea 6 g daily for four weeks and vice versa with a 2-week wash-out period. At the end of each period, a somatostatin-insulin-glucose infusion test (SIGIT) was performed to evaluate the insulin sensitivity. Fasting plasma glucose (FPG), HbA_1C, and oral glucose tolerance tests and insulin levels were measured before, during, and after the treatment.

Results. FPG and steady-state plasma glucose (SIGIT mean) were lower after GP treatment compared to placebo treatment (P < 0.001). The levels of FPG in the control group were slightly reduced to 0.2 ± 1.5 versus 1.9 ± 1.0 mmol/L in GP group (P < 0.001), and the effect on FPG was reversed after exchanging treatments. The glycometabolic improvements were achieved without any major change of circulating insulin levels. There were no changes in lipids, body measurements, blood pressure, and no reported hypoglycemias or acute adverse effects regarding kidney and liver parameters. Conclusion. The results of this study suggested that the GP tea exerted antidiabetic effect by improving insulin sensitivity.

[Darryl]

Zhu et al, 2017. Berberine treatment increases Akkermansia in the gut and improves high-fat diet-induced atherosclerosis in Apoe−/− mice. Atherosclerosis.

 

Apoe−/− mice were fed either a normal-chow diet or a high-fat diet (HFD). Berberine was administered to mice in drinking water (0.5 g/L) for 14 weeks. Gut microbiota profiles were established by high throughput sequencing of the V3–V4 region of the bacterial 16S ribosomal RNA gene. The effects of berberine on metabolic endotoxemia, tissue inflammation and gut barrier integrity were also investigated.

 

Berberine treatment significantly reduced atherosclerosis in HFD-fed mice. Akkermansia spp. abundance was markedly increased in HFD-fed mice treated with berberine. Moreover, berberine decreased HFD-induced metabolic endotoxemia and lowered arterial and intestinal expression of proinflammatory cytokines and chemokines. Berberine treatment increased intestinal expression of tight junction proteins and the thickness of the colonic mucus layer, which are related to restoration of gut barrier integrity in HFD-fed mice

 

 

[Benko]

I've been using (3g total 5:1 extract divided AM/PM) and recommending gynostemma extract for weight loss. 

 

Despite my fasting blood sugar of 87, and A1c of 5.5, I've known I'm insulin resistant because of my 40" waist and because "cheating" results in gaining back weight super easily.

 

My fasting insulin was just 17 microUI/ml.  I'll try to get some additional fasting insulin data and post it.

[YOLF]

So, anyone taking this stuff long term who wants to comment about their health history while on it?