Blood sugar lowering agents

JudoJosh

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This is strictly an informational thread so please keep product pimping down to a minimum as well as anecdotal remarks such as "XX product made me swole bro!".

Statements made in this are expected to be, at the very least based using some objective reasoning, but preferably if you have a reference, please share.
 
JudoJosh

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Bitter Melon

Effects of Momordica charantia on insulin resistance and visceral obesity in mice on high-fat diet☆

Abstract
We examined the preventive effect of Momordica charantia L. fruit (bitter melon) on hyperglycemia and insulin resistance in C57BL/6J mice fed with a high-fat (HF) diet. Firstly, mice were divided randomly into two groups: the control group was fed low-fat (LF) diet, whereas the experimental group was fed with a 45% HF diet last for 12 weeks. After 8 week of induction, the HF group was subdivided into six groups and was given orally with or without M. charantia or rosiglitazone 4 weeks afterward. We demonstrated that bitter melon was effective in ameliorating the HF diet-induced hyperglycemia, hyperleptinemia, and decreased the levels of blood glycated hemoglobin (HbA1c) and free fatty acid (FFA) (P<0.01, P<0.05, P<0.05, respectively), whereas increased the adipose PPARγ and liver PPARα mRNA levels. Additionally, bitter melon significantly decreased the weights of epididymal white adipose tissue and visceral fat, and decreased the adipose leptin and resistin mRNA levels. It is tempting to speculate that at least a portion of bitter melon effects is due to be through PPARγ-mediated pathways, resulting in lowering glucose levels and improving insulin resistance, and partly be through PPARα-mediated pathways to improve plasma lipid profiles. This is the first report demonstrating that bitter melon, is a food factor, but not a medicine, itself could influence dual PPARα/PPARγ expression and the mediated gene expression, is effective in ameliorating insulin resistance and visceral obesity
and as a plus it seems to have an effect on AMPK and PPAR-delta but I see no mention of fat loss but maybe this can be used in conjuction with something else that also activates AMPK so then possibly the bitter melon can enhance that activation and coupled with the glucose control aspect seem like a win win for body comp and health

Does bitter melon contain an activator of AMP-activated kinase?

Abstract
Extracts of the unripe fruit of Momordica charantia – bitter melon, which flourishes throughout the tropics – appear to have utility in the management of type 2 diabetes. Rodent studies suggest that the thus-far-uncharacterized active components of such extracts enhance the efficiency of postprandial glucose storage in muscle and liver, and likely diminish excessive hepatic glucose output, while often down-regulating serum insulin – effects comparable to those reported for metformin. Other parallels between the actions of metformin and bitter melon in rodents appear to include: analogous effects on the hepatic activity of certain enzymes of glucose metabolism; increased expression of GLUT4 in the plasma membrane of skeletal muscle; a tendency to prevent weight gain; favorable effects on serum lipids; and an anti-promotional impact on cancer induction. Inasmuch as the clinical efficacy of metformin has recently been traced to its ability to activate AMP-activated kinase, it would be of interest to determine whether bitter melon extracts contain activators of this enzyme. The fact that bitter melon has the potential to down-regulate insulin suggests that, beyond its likely utility in the management of diabetes, it may have preventive value with respect to a wide range of disorders in which hyperinsulinemia plays a pathogenic role – and possibly could even favorably impact the aging process
Activating effect of momordin, extract of bitter melon (Momordica Charantia L.), on the promoter of human PPARdelta.

Abstract
AIM: Bitter melon (Momordica charantia L.) is a common vegetable grown in Okinawa that has also been used recently in medicine for the treatment of diseases such as diabetes, hypertension, and dyslipidemia. Among Bitter melon extracts compounds, we focused on an extract known as momordin in the present study, to examine its effect on peroxisome-proliferator activated-receptor (PPAR) delta (also called PPARdelta in rodents) expression and promoter activity of the human PPARdelta gene. METHODS: A human PPARdelta promoter-reporter plasmid was made as a template from a BAC CLONE (RPCI-11C) containing a -3076 bp (BglI site) +74 bp (EcoRI site) sequence. Luciferase assay of PPARdelta promoter activity was performed using HepG2 cells. RESULTS: 10 and 25 nM Momordin significantly increased the expression of PPARdelta mRNA 1.5-fold (relative to the control). Moreover, 10 and 25 nM Momordin significantly increased PPARdelta promoter activity in a dose-dependent manner, reaching more than 1.5-fold relative to the control. CONCLUSION: Our present data obtained through successful cloning of the PPARdelta promoter demonstrate that PPARdelta production and activation are upregulated through PPARdelta promoter activity following momordin treatment.
Antidiabetic Activities of Triterpenoids Isolated from Bitter Melon Associated with Activation of the AMPK Pathway

Summary
Four cucurbitane glycosides, momordicosides Q, R, S, and T, and stereochemistry-established karaviloside XI, were isolated from the vegetable bitter melon (Momordica charantia). These compounds and their aglycones exhibited a number of biologic effects beneficial to diabetes and obesity. In both L6 myotubes and 3T3-L1 adipocytes, they stimulated GLUT4 translocation to the cell membranean essential step for inducible glucose entry into cells. This was associated with increased activity of AMP-activated protein kinase (AMPK), a key pathway mediating glucose uptake and fatty acid oxidation. Furthermore, momordicoside(s) enhanced fatty acid oxidation and glucose disposal during glucose tolerance tests in both insulin-sensitive and insulin-resistant mice. These findings indicate that cucurbitane triterpenoids, the characteristic constituents of M. charantia, may provide leads as a class of therapeutics for diabetes and obesity
but then with the good comes the bad. Supposedly there is a connection between bitter melon with liver toxicity and fertility issues. Can anyone get this FT - http://www.ncbi.nlm.nih.gov/pubmed/12625217 ?
 
JudoJosh

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Oh and this doesnt sound like a good thing

Inhibition of protein synthesis in vitro by proteins from the seeds of Momordica charantia (bitter pear melon).

Abstract.

A haemagglutinating lectin was purified from the seeds of Momordica charantia by affinity chromatography on Sepharose 4B and on acid-treated Sepharose 6B. It has mol.wt. 115 000 and consists of four subunits, of mol.wts. 30 500, 29 000, 28 500 and 27 000. 2. The lectin inhibits protein synthesis by a rabbit reticulocyte lysate with an ID50 (concentration giving 50% inhibition) of approx. 5 micrograms/ml. Protein synthesis by Yoshida ascites cells is partially inhibited by the lectin at a concentration of 100 micrograms/ml. 3. From the same seeds another protein was purified which has mol.wt. 23 000 and is a very potent inhibitor of protein synthesis in the lysate system, with an ID50 of 1.8 ng/ml. This inhibitor has no effect on protein synthesis by Yoshida cells, and has no haemagglutinating properties. 4. Artemia salina ribosomes preincubated with the lectin or with the inhibitor lose their capacity to perform protein synthesis. The proteins seem to act catalytically, since they inactivate a molar excess of ribosomes. 5. The lectin and the inhibitor are somewhat toxic to mice, the LD50 being 316 and 340 micrograms/100 g body wt. respectively.
FT - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1161595/

But I am not too convinced this would happen with BM as the above uses a purified extract of lectin from the fruit and not the whole fruit (which in theory should have less lectin per dose)
 
JudoJosh

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Coop? EBF? This seems right up you guys alley ;)
 

mr.cooper69

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Yeah I love researching this stuff. Busy with some readings at the moment and I've had a very long day, but I'll try to contribute tomorrow.
 
JudoJosh

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Speak of the devil ;)
 
Mainevant

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Here are 3 studies contains: 4-hydroxyisoleucine, Gymnema Sylvestre, Cinnamon Extract.

The plant fenugreek has been used for centuries as a treatment for diabetes. This article presents evidence that the major isomer of 4-hydroxyisoleucine, an atypical branched-chain amino acid derived from fenugreek, is responsible for the effects of this plant on glucose and lipid metabolism. 4-Hydroxyisoleucine was demonstrated to stimulate glucose-dependent insulin secretion by a direct effect on pancreatic islets. In addition to stimulating insulin secretion, 4-hydroxyisoleucine reduced insulin resistance in muscle and/or liver by activating insulin receptor substrate-associated phosphoinositide 3 (PI3) kinase activity. 4-Hydroxyisoleucine also reduced body weight in diet-induced obese mice. The decrease in body weight was associated with a marked decrease in both plasma insulin and glucose levels, both of which are elevated in this animal model. Finally, 4-hydroxyisoleucine decreased elevated plasma triglyceride and total cholesterol levels in a hamster model of diabetes. Based on the beneficial metabolic properties that have been demonstrated, 4-hydroxyisoleucine, a simple, plant-derived amino acid, may represent an attractive new candidate for the treatment of type 2 diabetes, obesity and dyslipidemia, all key components of metabolic syndrome.

Many plant-based products have been suggested as potential antidiabetic agents, but few have been shown to be effective in treating the symptoms of Type 2 diabetes mellitus (T2DM) in human studies, and little is known of their mechanisms of action. Extracts of Gymnema sylvestre (GS) have been used for the treatment of T2DM in India for centuries. The effects of a novel high molecular weight GS extract, Om Santal Adivasi, (OSA(R)) on plasma insulin, C-peptide and glucose in a small cohort of patients with T2DM are reported here. Oral administration of OSA(R) (1 g/day, 60 days) induced significant increases in circulating insulin and C-peptide, which were associated with significant reductions in fasting and post-prandial blood glucose. In vitro measurements using isolated human islets of Langerhans demonstrated direct stimulatory effects of OSA(R) on insulin secretion from human ß-cells, consistent with an in vivo mode of action through enhancing insulin secretion. These in vivo and in vitro observations suggest that OSA(R) may provide a potential alternative therapy for the hyperglycemia associated with T2DM.

The aim of this study was to determine whether cinnamon extract (CE) would improve the glucose utilization in normal male Wistar rats fed a high-fructose diet (HFD) for three weeks with or without CE added to the drinking water (300 mg/kg/day). In vivo glucose utilization was measured by the euglycemic clamp technique. Further analyses on the possible changes in insulin signaling occurring in skeletal muscle were performed afterwards by Western blotting. At 3 mU/kg/min insulin infusions, the decreased glucose infusion rate (GIR) in HFD-fed rats (60 % of controls, p < 0.01) was improved by CE administration to the same level of controls (normal chow diet) and the improving effect of CE on the GIR of HFD-fed rats was blocked by approximately 50 % by N-monometyl-L-arginine. The same tendency was found during the 30 mU/kg/min insulin infusions. There were no differences in skeletal muscle insulin receptor (IR)-beta, IR substrate (IRS)-1, or phosphatidylinositol (PI) 3-kinase protein content in any groups. However, the muscular insulin-stimulated IR-beta and IRS-1 tyrosine phosphorylation levels and IRS-1 associated with PI 3-kinase in HFD-fed rats were only 70 +/- 9 %, 76 +/- 5 %, and 72 +/- 6 % of controls (p < 0.05), respectively, and these decreases were significantly improved by CE treatment. These results suggest that early CE administration to HFD-fed rats would prevent the development of insulin resistance at least in part by enhancing insulin signaling and possibly via the NO pathway in skeletal muscle.
 
JudoJosh

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Here are 3 studies contains: 4-hydroxyisoleucine, Gymnema Sylvestre, Cinnamon Extract.




I think the 4-hydroxyisoleucine has some potential but after speaking to a couple formulators, apparently it is difficult to obtain.

As for the cinnamon, the data on it is conflicting so it isnt as clear if it is or how effective it is.

On one hand you have studies like the one you posted above and ones like http://www.ncbi.nlm.nih.gov/pubmed/14625128 Which suggest it can improve the function of insulin

But then you have

http://care.diabetesjournals.org/content/31/1/41.abstract

Do you have an opinion cinnamon?
 
rob112

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In on thread. At a phone so no way to really contribute as of now :(

Judo, I have noticed a lot of GDA/insulin mimics also promote tumor apoptosis when I research it. Is that side of things worth mention in this thread? I may be way off here, but is too far fetched that onset of type 2 or any type of insulin related problems increase cancer risks?
 
Mainevant

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I think that Cinnamon is effective..

4-hydroxyisoleucine extracted from Fenugreek has nice opinions on net.

For me the most innovative insulinmimetric supps are:
Gymnema Sylvestre (standardized to a minimum of 25% gymnemic acid)
Lagerstroemia Speciosa (source of corosolic acid)
 
MAxximal

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Punica Granatum Extract

Active Ingredient : Ellagic Acid 20%, Ellagic Acid 40% & Tannins 25%

Common Name : Pomegranate

Chemical Constituents and Components : Main chemical constitutes are punicalagin, ellagic acid, luteolin, quercetin, kaempferol, ellagitannins, anthocyanins (delphinidin, cyanidin, and pelargonidin) and EA-glycosides

Peroxisome proliferator-activated receptor (PPAR)-gamma activators are widely used in the treatment of type 2 diabetes because they improve the sensitivity of insulin receptors.

http://www.ncbi.nlm.nih.gov/pubmed/16102567
 
AZMIDLYF

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CJ_Xfit89

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I think that Cinnamon is effective..

4-hydroxyisoleucine extracted from Fenugreek has nice opinions on net.

For me the most innovative insulinmimetric supps are:
Gymnema Sylvestre (standardized to a minimum of 25% gymnemic acid)
Lagerstroemia Speciosa (source of corosolic acid)
Banaba at 20% is effective.
 
CJ_Xfit89

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Opinions on HCA & berberine?
Work well.
HCA blocks absorption of fat and adipocytes.
Berberine boosts AMPk. DO NOT fear expression of atrogin-1 as this is prevalant in diabetic patients and not so much for the general low inflammed type people
 
Smitty77

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I think the 4-hydroxyisoleucine has some potential but after speaking to a couple formulators, apparently it is difficult to obtain.

As for the cinnamon, the data on it is conflicting so it isnt as clear if it is or how effective it is.

On one hand you have studies like the one you posted above and ones like http://www.ncbi.nlm.nih.gov/pubmed/14625128 Which suggest it can improve the function of insulin

But then you have

http://care.diabetesjournals.org/content/31/1/41.abstract

Do you have an opinion cinnamon?
Great thread, Josh!

4-OH isoleucine isn't so much hard to obtain as it's quite expensive to source.

We were going to consider cinnamon at first, but the research is almost 50/50 and couldn't necessarily bank on that... I think it would have its place amongst a more comprehensive formula, but in a primary ingredient capacity, I think emerging research has to lean a bit more to the favorable side.

I'll also throw out Gynostemma/jiaogulan, because the research was quite impressive (even beyond antidiabetic effects):
http://www.ncbi.nlm.nih.gov/pubmed/20213586
http://www.ncbi.nlm.nih.gov/pubmed/15220351
 

mr.cooper69

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Work well.
HCA blocks absorption of fat and adipocytes.
Berberine boosts AMPk. DO NOT fear expression of atrogin-1 as this is prevalant in diabetic patients and not so much for the general low inflammed type people
Re-check some of the info in this post.

I'm obviously big on Na-RLA, but I think there is a lot of unexplored territory as far as herbs go. Your mind would be blown at how many traditional plant extracts have anti-diabetic/hypoglycemic effects. There is one in particular that is very expensive but incredibly effective.
 

uvawahoowa

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Punica Granatum Extract

Active Ingredient : Ellagic Acid 20%, Ellagic Acid 40% & Tannins 25%

Common Name : Pomegranate

Chemical Constituents and Components : Main chemical constitutes are punicalagin, ellagic acid, luteolin, quercetin, kaempferol, ellagitannins, anthocyanins (delphinidin, cyanidin, and pelargonidin) and EA-glycosides

Peroxisome proliferator-activated receptor (PPAR)-gamma activators are widely used in the treatment of type 2 diabetes because they improve the sensitivity of insulin receptors.

http://www.ncbi.nlm.nih.gov/pubmed/16102567
What would be a serving size for this? For say 100g of carbs? Just curious to see if it would be cost effective to add to my stack
 

uvawahoowa

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Work well.
HCA blocks absorption of fat and adipocytes.
Berberine boosts AMPk. DO NOT fear expression of atrogin-1 as this is prevalant in diabetic patients and not so much for the general low inflammed type people
So would HCA be best taken before a high fat meal rather than a high carb meal? Or am I reading that wrong?
 

broons

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Re-check some of the info in this post.

I'm obviously big on Na-RLA, but I think there is a lot of unexplored territory as far as herbs go. Your mind would be blown at how many traditional plant extracts have anti-diabetic/hypoglycemic effects. There is one in particular that is very expensive but incredibly effective.
Could you shed some light on the very expensive extract?
 

Greenhulk

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Alpha-lipoic acid. The following studies although only performed on diabetic patients suggest that it may lower blood glucose levels.

Arzneimittelforschung. 1995 Aug;45(8):872-4.
Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid.
Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, Dietze GJ.
Source

Department of Internal Medicine, City Hospital, Baden-Baden, Germany.
Abstract

Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore pharmacological interventions should aim to improve insulin sensitivity. Alpha-lipoic acid (CAS 62-46-4, thioctic acid, ALA), a natural occurring compound frequently used for treatment of diabetic polyneuropathy, enhances glucose utilization in various experimental models. To see whether this compound also augments insulin mediated glucose disposal in NIDDM, 13 patients received either ALA (1000 mg/Thioctacid/500 ml NaCl, n = 7) or vehicle only (500 ml NaCl, n = 6) during a glucose-clamp study. Both groups were comparable in age, body-mass index and duration of diabetes and had a similar degree of insulin resistance at baseline. Acute parenteral administration of ALA resulted in a significant increase of insulin-stimulated glucose disposal; metabolic clearance rate (MCR) for glucose rose by about 50% (3.76 ml/kg/min = pre vs. 5.82 ml/kg/min = post, p < 0.05), whereas the control group did not show any significant change (3.57 ml/kg/min = pre vs. 3.91 ml/kg/min = post). This is the first clinical study to show that alpha-lipoic acid increases insulin stimulated glucose disposal in NIDDM. The mode of action of ALA and its potential use as an antihyperglycemic agent require further investigation.
Free Radic Biol Med. 1999 Aug;27(3-4):309-14.
Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial.
Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, Rett K.
Source

Hypertension and Diabetes Research Unit, Max Grundig Clinic, Bühl and City Hospital, Baden-Baden, Germany.

Abstract

Alpha-lipoic acid (ALA), a naturally occuring compound and a radical scavenger was shown to enhance glucose transport and utilization in different experimental and animal models. Clinical studies described an increase of insulin sensitivity after acute and short-term (10 d) parenteral administration of ALA. The effects of a 4-week oral treatment with alpha-lipoic acid were evaluated in a placebo-controlled, multicenter pilot study to determine see whether oral treatment also improves insulin sensitivity. Seventy-four patients with type-2 diabetes were randomized to either placebo (n = 19); or active treatment in various doses of 600 mg once daily (n = 19), twice daily (1200 mg; n = 18), or thrice daily (1800 mg; n = 18) alpha-lipoic acid. An isoglycemic glucose-clamp was done on days 0 (pre) and 29 (post). In this explorative study, analysis was done according to the number of subjects showing an improvement of insulin sensitivity after treatment. Furthermore, the effects of active vs. placebo treatment on insulin sensitivity was compared. All four groups were comparable and had a similar degree of hyperglycemia and insulin sensitivity at baseline. When compared to placebo, significantly more subjects had an increase in insulin-stimulated glucose disposal (MCR) after ALA treatment in each group. As there was no dose effect seen in the three different alpha-lipoic acid groups, all subjects receiving ALA were combined in the "active" group and then compared to placebo. This revealed significantly different changes in MCR after treatment (+27% vs. placebo; p < .01). This placebo-controlled explorative study confirms previous observations of an increase of insulin sensitivity in type-2 diabetes after acute and chronic intravenous administration of ALA. The results suggest that oral administration of alpha-lipoic acid can improve insulin sensitivity in patients with type-2 diabetes. The encouraging findings of this pilot trial need to be substantiated by further investigations.
Hormones (Athens). 2006 Oct-Dec;5(4):251-8.
Improvement of insulin sensitivity in patients with type 2 diabetes mellitus after oral administration of alpha-lipoic acid.
Kamenova P.
Source

Department of Diabetology, University Hospital of Endocrinology, Medical University, Sofia, Bulgaria.
Abstract

BACKGROUND:
Amelioration of insulin resistance could improve both glycaemic control and cardiovascular risk factors in patients with type 2 diabetes mellitus. Alpha-lipoic acid has been shown to improve insulin action after parenteral administration.

OBJECTIVE:
the aim of the study was to assess the effect of oral administration of alpha-lipoic acid on insulin sensitivity in patients with type 2 diabetes.

DESIGN:
twelve patients (mean+/-sD; age 52.9+/-9.9 yrs; body mass index 33.9+/-7.4 kg/m(2)) were treated with oral alpha-lipoic acid, 600 mg twice daily over a period of 4 weeks. twelve subjects with normal glucose tolerance served as a control group in terms of insulin sensitivity (Is). Is was measured by a 2h manual hyperinsulinaemic (insulin infusion rate-40 mU/m(2 )body surface area/min) euglycaemic (blood glucose kept at 5 mmol/l) clamp technique and expressed as a glucose disposal rate (M) and insulin sensitivity index (IsI).

RESULTS:
At the end of the treatment period, Is of diabetic patients was significantly increased: M from 3.202+/-1.898 to 5.951+/-2.705 mg/kg/min (mean+/-sD), p<0.01; and IsI from 4.706+/-2.666 to 7.673+/-3.559 mg/kg/min per mIU/l x 100 (mean+/-sD), p<0.05. the difference was not statistically significant between the Is of diabetic patients after alpha-lipoic acid therapy and control subjects.

CONCLUSION:
short-term oral alpha-lipoic acid treatment increases peripheral insulin sensitivity in patients with type 2 diabetes mellitus.
 

Greenhulk

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Vanadyl sulfate may be another blood sugar lowering agent. Here are the studies supporting this, however, again in the context of diabetes. So, we can't really tell how this translates to healthy human beings.

Biochem Biophys Res Commun. 1993 Dec 30;197(3):1549-55.
Studies of vanadyl sulfate as a glucose-lowering agent in STZ-diabetic rats.
Thompson KH, Leichter J, McNeill JH.
Source

Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
Abstract

To study the effect of vanadium (V) intake on blood glucose lowering, tissue V concentrations, glutathione reductase (GR) activity, and plasma trace metal concentrations, streptozotocin(STZ)-diabetic rats were treated with vanadyl sulfate (VS) (0.5-1.2 g/l in the drinking water) for up to 12 weeks. Kidney and plasma V concentrations were positively correlated with V intake. Kidney GR activities were not affected by VS treatment nor were plasma cobalt, molybdenum, manganese or lithium concentrations. Individual V intakes were dependent upon severity of diabetes, with more hyperglycemic rats consuming greater quantities of VS solution. A diminished effect on glucose lowering of VS above 1 g/l was noted.
Metabolism. 1996 Sep;45(9):1130-5.
Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus.
Boden G, Chen X, Ruiz J, van Rossum GD, Turco S.
Source

Division of Endocrinology/Diabetes/Metabolism and the General Clinical Research Center, Temple University Schools of Medicine and Pharmacy, Philadelphia, PA, USA.
Abstract

The safety and efficacy of vanadyl sulfate (VS) was tested in a single-blind, placebo-controlled study. Eight patients (four men and four women) with non-insulin-dependent diabetes mellitus (NIDDM) received VS (50 mg twice daily orally) for 4 weeks. Six of these patients (four men and two women) continued in the study and were given a placebo for an additional 4 weeks. Euglycemic-hyperinsulinemic clamps were performed before and after the VS and placebo phases. VS was associated with gastrointestinal side effects in six of eight patients during the first week, but was well tolerated after that. VS administration was associated with a 20% decrease in fasting glucose concentration (from 9.3 +/- 1.8 to 7.4 +/- 1.4 mmol/L, P < .05) and a decrease in hepatic glucose output (HGO) during hyperinsulinemia (from 5.0 +/- 1.0 pre-VS to 3.1 +/- 0.9 micromol/kg x min post-VS, P < .02). The improvement in fasting plasma glucose and HGO that occurred during VS treatment was maintained during the placebo phase. VS had no significant effects on rates of total-body glucose uptake, glycogen synthesis, glycolysis, carbohydrate (CHO) oxidation, or lipolysis during euglycemic-hyperinsulinemic clamps. We conclude that VS at the dose used was well tolerated and resulted in modest reductions of fasting plasma glucose and hepatic insulin resistance. However, the safety of larger doses and use of vanadium salts for longer periods remains uncertain.
 
JudoJosh

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In on thread. At a phone so no way to really contribute as of now :(

Judo, I have noticed a lot of GDA/insulin mimics also promote apoptosis when I research it. Is that side of things worth mention in this thread? I may be way off here, but is too far fetched that onset of type 2 or any type of insulin related problems increase cancer risks?
i say it is definitely worth discussing, but I am unsure of how much of an discussion we can really have on it. Personally, I havent come across research that connected them to cancer but I assume these are correlations? If so we would have to examine the extent of the relationship. Or are they in vitro studies? The problems which arise with these are that bathing a cell with a substance in a petri dish can only tell us so much on how it will act in vivo. But ultimately the problem with discussing potential cancer risk are their are a ton of unknowns with cancer. Genetic susceptibility plays a big role here as the enzyme that is responsible for triggering cellular apoptosis, when it goes haywire you have cancer and some individuals are genetically protected from it while others arent. All in all it is a tricky subject but certainly worth at least talking about but specifics will probably be beyond the scope of our community here.


Edit: sorry I am on the phone and I completely misread your post. I see now you are suggesting these ingredients might be "anti cancer" and I initially read it as "pro cancer". My bad :)
 

Clemenza

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Vanadyl sulfate may be another blood sugar lowering agent. Here are the studies supporting this, however, again in the context of diabetes. So, we can't really tell how this translates to healthy human beings.
I've run blood glucose tests using just about every gda we've mentioned and haven't found anything close to being as effective as Vanadyl Sulfate.

It is overlooked IMO and if you dig deep in the research you will find it is not toxic in recommended dosing.
 
rob112

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Edit: sorry I am on the phone and I completely misread your post. I see now you are suggesting these ingredients might be "anti cancer" and I initially read it as "pro cancer". My bad :)
I haven't gotten to in a minute, but every time I started digging on GDA type supplements I always came across tumor apoptosis. If I get time to really look on my PC I'll post up some stuff.
 
JudoJosh

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Opinions on HCA & berberine?
EBF is the guy to talk to about HCA. He is a big fan of the stuff and I dont know much about it. There used to be another guy who posted here and was an advocate of its use but I havent seen him in a while and cant remember his username.

I am a fan of berberine personally but will admit there is some questionable issues with its use.

Berberine boosts AMPk.
I am unsure to what extent it actually does. It is not clear that berberine taken orally would reach the blood concentrations that it does in some of the in-vitro studies.

DO NOT fear expression of atrogin-1 as this is prevalant in diabetic patients and not so much for the general low inflammed type people
I somewhat agree. I do not fear berberine based of the atrogin study either but I dont feel it is something we can just dismiss because of the study design. While the study used diabetic mice and their effects do not necessarily transfer to what happens in humans, it still isnt enough to just dismiss a potential negative side effect. But again this isnt something I really fear as their are enough anecdotal reports that make me feel better about its use.

Now question, isnt AMPK a stimulator of atrogin-1 expression in muscle? See - http://ajpendo.physiology.org/content/292/6/E1555.full

So couldnt this increase in atrogin-1 expression simply be from the activating AMPK via the use of berberine?

Overall even if berberine did suppress protein synthesis, i think this transient effect wont actually result in a quantitative difference with regards to ones lean body mass over time.

Also to note, while we are on the discussion of berberine it does appear to also result in an inhibition of liver enzymes which may lead to other health problems and/or an interaction with other supplementation/medication - http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=cytochrome
 
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Apple Cider Vingear Organic with the Mother. Cheap and effective.
 
louiefci

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first off i'd like to say that this is a very good thread, i've been doing some hardcore research on this for the past week or so. I've been noticing a big difference in my body, im getting really lean and cut up everywhere except for one area on my body and that is my lower abdominal area. i have abs but that little chuck of **** just wont go away! i eat very clean, i play in a soccer league, jog and weight train. My friend told me it could be that my insulin sensitivity is f*****. i did some research and came up with 2 possible answers.. like i stated before, insulin resistance or my cortisol levels are shot. im going to start a little experiment and hopefully find out what the problem is so i could fix it ASAP! if you guys have any advice on this, your help would definitely be appreciated!

back on point.. i found a doctor that tested a few supplements on insulin resistant patients.... heres the info:

Supplements

What about supplements such as Chromium?

All of my diabetics go on 1,000 mcg of chromium, some a little bit more if they are really big people. The amount is usually 500 mcg for a non-diabetic, though it depends on their insulin levels.

I use a lot of supplements. What you really want to do is to try to convert the person back into being an efficient burner of fat. Earlier we talked about when you are very insulin resistant and you are waking up in the morning with an insulin level that is elevated, you cannot burn fat but instead are burning sugar.

One of the reasons that sugar goes up so high is because that is what your cell is needing to burn, but if it is so insulin resistant it requires a blood sugar of 300 so that just by mass action some can get into the cell and be used as fuel. If you eliminate that need to burn sugar, you don't need such high levels of sugar even if you are insulin resistant.

You want to increase the ability of the cells in the body to burn fat and make that glucose burner into a fat burner. You want to make a gasoline-burning car into a diesel-burning car. Did anyone ever look at the molecular structure of diesel fuel in your spare time? It looks almost identical to a fatty acid. There is a company right now that can tell you how to alter vegetable oil to use in your Mercedes. It's just a matter of thinning it out a little bit. It is a very efficient fuel.

Triglycerides

You can look at other variables that will give you some idea too, such as triglycerides. If people are very sensitive to high levels of insulin, they come in with insulin levels of 14 and they have triglycerides of 1000. You would treat them just as you would if they had an insulin level of 50. It gives you some idea of the effect of the hyperinsulinemia on the body.

You can use triglycerides as a gauge, which I often do. The objective is to try to get the insulin level just as low as you possibly can. There is no limit. They classify diabetes now as a fasting blood sugar of 126 or higher. A few months ago it might have been 140. It is just an arbitrary number. Does that mean that someone with a blood sugar of 125 is non-diabetic and fine? If you have a blood sugar of 125 you are worse than if you had a blood sugar of 124--same with insulin. If you have a fasting insulin of 10, you are worse off than if you had an insulin of 9. You want to get it just as low as you can.

Does This Apply to Athletes?

With athletes, think about the effect of carbohydrate loading before an event. What happens if you eat a bowl of pasta before you have to run a marathon? What does that bowl of pasta do? It raises your insulin. What is the instruction of insulin to your body?

To store energy and not burn it. I see a fair amount of athletes and this is what I tell them, you want everybody, athletes especially, to be able to burn fat efficiently. So when they train, they are on a very low-carbohydrate diet. The night before their event, they can stock up on sugar and load their glycogen if they would like.

They are not going to become insulin resistant in one day. Just enough to make sure, it has been shown that if you eat a big carbohydrate meal that you will increase your glycogen stores, that is true and that is what you want. But you don't want to train that way because if you do you won't be able to burn fat, you can only burn sugar, and if you are an athlete you want to be able to burn both.

Few people have problems burning sugar if they are athletes, but they have lots of problems burning fat, so they hit the wall. And for certain events, like sprinting, it is less important, truthfully for their health it is very important to be able to burn fat, but a sprinter will go right into burning sugar. If you are a 50-yard dash person, whether you can burn fat or not is not going to make a huge difference in your final performance.

Beyond your athletic years, if you don't want to become a diabetic, and don't want to die of heart disease and don't want to age quickly, it is certainly not going to do you any harm to be able to burn fat efficiently in addition to sugar.

Vanadyl Sulfate

Vanadyl Sulfate is an insulin mimic, so that it can basically do what insulin does by a different mechanism. If it went through the same insulin receptors, then it wouldn't offer any benefit, but it doesn't, it actually has been shown to go through a different mechanism to lower blood sugar, so it spares insulin and then it can help improve insulin sensitivity. To really lower a person’s insulin, I give 25 mg 3 times a day temporarily.

Glutamine Powder

I also put people on glutamine powder. Glutamine can act as a brain fuel, so it helps eliminate carbohydrate cravings while they are in that transition period. I like to give it to them at night, and I tell them to use it whenever they feel they are craving carbohydrates. They can put several grams into a little water and drink it and it helps eliminate carbohydrate cravings between meals.

A high-protein diet will increase an acid load in the body, but not necessarily a high-fat diet. Vegetables and greens are alkalinizing, so if you are eating a lot of vegetables along with your protein it equalizes the acidifying effect of the protein. I don't recommend a high-protein diet; I recommend an adequate protein diet.
i found another doctor(Dr. Jen Morganti) that uses spices/spice extracts and vitamins to restore her patients sugar levels:

After establishing a solid foundation of healthy foods, add some herbs and nutrients that act to diminish inflammation and potentially improve insulin sensitivity. The herbal extract curcumin, derived from the tasty Indian spice turmeric, has been the subject of thousands of studies. One of the known super powers possessed by curcumin is it’s antiinflammatory activity, which, among other things, may effectively improve cells’ sensitivity to insulin and lower blood sugar levels.
A second delicious spice that helps prevent insulin resistance is cinnamon extract. There have been some conflicting studies about cinnamon’s role, but on a positive note, certain cinnamon extracts have been shown to reduce secretion of inflammatory cytokines from fat cells. By decreasing overall inflammation, cells become more sensitive to insulin. Cinnamon has also been shown in studies to reduce the amount of insulin released after eating, and helps keep blood sugar levels balanced. You can benefit from adding cinnamon to food on a daily basis, and take a standardized extract in pill form.
The recent plethora of vitamin D research has helped establish its potent anti-inflammatory actions, so it comes as no surprise to find that vitamin D deficiency is related to increased risk of developing Type 2 diabetes. A few studies have suggested that supplementing with vitamin D may improve insulin resistance. Anyone struggling to fend off diabetes should take a simple vitamin D blood test, setting a goal of over 50 dl/ml. That goal becomes more achievable when supplementing with 2,000- 5,000 IU of vitamin D a day.
Ultimately, inflammation is at the root of insulin resistance and diabetes. The key to prevention is dietary modification and supplementation to aid in weight loss and decreased inflammation. Under these conditions, insulin resistance can be reversed and blood sugar levels normalized.
hope this info help! i'll be following this thread for a long time :) i cant wait to start my little experiment ehehehehe
 
nattydisaster

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Number 1 flaw in these types of ingredients:

Companies pimp ingredients that show to work wonders in diabetic animal models, but do absolutely nothing in normal animal models. For bodybuilding purposes, you need it to work in the normal animal model
 

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Number 1 flaw in these types of ingredients:

Companies pimp ingredients that show to work wonders in diabetic animal models, but do absolutely nothing in normal animal models. For bodybuilding purposes, you need it to work in the normal animal model
This precisely. Russian taragon bro!
 
louiefci

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Number 1 flaw in these types of ingredients:

Companies pimp ingredients that show to work wonders in diabetic animal models, but do absolutely nothing in normal animal models. For bodybuilding purposes, you need it to work in the normal animal model
Good point, that's why I tried to find doctor recommend supplements/ingredients that were actually tested on humans with & without diabetes!
 
louiefci

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This precisely. Russian taragon bro!
you seem to be right, Russian tarragon was tested on NON DIABETIC humans the results were great! heres the info:

Background: Russian tarragon extracts have been reported to have anti-diabetic activity in animals. This pilot study aimed to investigate the acute effects of an aqueous extract of Russian tarragon (RT) on serum glucose and insulin in response to an oral glucose tolerance test (OGTT).
Methods: Using a randomized, double-blind, cross-over design, 12 non-diabetic men reported to the lab on 2 different mornings separated by 1 to 2 weeks, and ingested 75 g of dextrose in solution. Fifteen minutes before ingestion, subjects ingested either 2 g of RT or a placebo. Blood samples were collected before ingestion of the RT and placebo, and at 15, 30, 45, 60, and 75 minutes post ingestion of the dextrose load. Samples were assayed for serum glucose and insulin.
Results: For serum glucose, no condition (P = 0.19) or condition × time (P = 0.99) effect was noted. A time effect was noted (P < 0.0001), with values at 15 and 30 minutes higher than pre-ingestion (P < 0.05). No area under the curve (AUC) effect (P = 0.54) was noted, although a 4.5% reduction in AUC was observed for RT (569 ± 92 mg · dL−1 · 75 min−1) vs placebo (596 ± 123 mg · dL−1 · 75 min−1). Similar findings were noted for serum insulin, with no condition (P = 0.24) or condition × time (P = 0.98) effect noted. A time effect was noted (P < 0.0001), with values at 15, 30, and 45 minutes higher than pre-ingestion (P < 0.05). No AUC effect (P = 0.53) was noted, although a 17.4% reduction in AUC was observed for RT (114 ± 22 µIU · mL−1 · 75 min−1) vs placebo (138 ± 30 µIU · mL−1 · 75 min−1). Approximately two-thirds of subjects ingesting the RT experienced attenuation in both the glucose and insulin response to the OGTT.
Conclusion: These data indicate that acute ingestion of RT results in a slight, non-statistically significant lowering of blood glucose in response to a dextrose load. This occurs in the presence of a slightly lower insulin response. These findings are specific to a small sample of healthy, non-diabetic men. Additional study is needed involving a larger sample of individuals with pre-diabetes or untreated diabetes.
 
JudoJosh

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Punica Granatum Extract

Active Ingredient : Ellagic Acid 20%, Ellagic Acid 40% & Tannins 25%

Common Name : Pomegranate

Chemical Constituents and Components : Main chemical constitutes are punicalagin, ellagic acid, luteolin, quercetin, kaempferol, ellagitannins, anthocyanins (delphinidin, cyanidin, and pelargonidin) and EA-glycosides

Peroxisome proliferator-activated receptor (PPAR)-gamma activators are widely used in the treatment of type 2 diabetes because they improve the sensitivity of insulin receptors.

http://www.ncbi.nlm.nih.gov/pubmed/16102567
Pomegranate also contains a nice amount of CLnA which has lots of positive health related benefits http://www.springerlink.com/content/l70k381563060g77/ (need FT access)


Thanks, although I am not sure how much this will actually help with fat loss. Never really heard of any reports to confirm this (unlike with berberine)

Re-check some of the info in this post.

I'm obviously big on Na-RLA, but I think there is a lot of unexplored territory as far as herbs go. Your mind would be blown at how many traditional plant extracts have anti-diabetic/hypoglycemic effects. There is one in particular that is very expensive but incredibly effective.
How do you feel about Na-rALA vs just bulk ALA?

When dosed high enough I feel bulk ALA is more cost effective
 
nattydisaster

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So far I have found it does not change my fasting glucose levels but it is great when used with meals

Small dose needed too which is nice
 

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Pomegranate also contains a nice amount of CLnA which has lots of positive health related benefits (need FT access)




Thanks, although I am not sure how much this will actually help with fat loss. Never really heard of any reports to confirm this (unlike with berberine)



How do you feel about Na-rALA vs just bulk ALA?

When dosed high enough I feel bulk ALA is more cost effective
I believe we had this discussion earlier:

If only it were so simple. Na-R-ALA is actually a better deal when you account for numerous factors.

<- Read it all when you get the chance. Helped tremendously in writing my research review.

Of note:

"Cmax and AUC values for NaRLA in the male subject were 25.86 and 3.3 times higher, respectively, than RLA."
"
The current study and previous findings from this laboratory conclude that pure RLA is not suitable for use in nutraceutical or pharmaceutical products. Rather, it should be treated as raw material for further processing into stable, bioavailable dosage forms. PK data reveals pure RLA is significantly less bioavailable than RLA found as a 50-percent component of rac-LA; and RLA in a salt form is considerably more bioavailable than an equivalent dose of racLA (RLA + SLA). This indicates SLA may function as a competitive inhibitor in the absorption of RLA."

If quality is accounted for, Na-R-ALA is the way to go from a cost:benefit perspective.
You went MIA around this time :(
 
Mainevant

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I think I will try it on myself.
You have 4-hydroxyleucine extracted from Fenugreek or other source?
How much of it are you taking?
 
JudoJosh

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Any opinions on the slinshot actives?
Please see the first post in this thread as this is not an acceptable question here.

There is no room for discussing specific products. If you want to talk about ingredients, their MOAs and possible synergy between other glucose control adiuvants, then that is fine. But if you want to ask about a product specifically, please do so in another thread

Thank you for your understanding
 
louiefci

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Any opinions on the slinshot actives?
the main ingredient in slinshot is Artemisia Dracunculus L. var. inodora, also and better known as Russian tarragon. if you go back to the second page of this thread, you'll see a comment left by me with results from a test done on 12 non diabetic humans taking russian tarragon.

by the way slinshot is a great product, nothing but positive reviews! ill put down some links so you could see for yourself!

http://supplementreviews.com/purus-labs/slinshot
http://www.nutraplanet.com/product/purus-labs/slinshot-90-capsules.html
 
louiefci

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Please see the first post in this thread as this is not an acceptable question here.

There is no room for discussing specific products. If you want to talk about ingredients, their MOAs and possible synergy between other glucose control adiuvants, then that is fine. But if you want to ask about a product specifically, please do so in another thread

Thank you for your understanding
oh krap i just saw your comment now, im sorry for my last post!
 

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the main ingredient in slinshot is Artemisia Dracunculus L. var. inodora, also and better known as Russian tarragon. if you go back to the second page of this thread, you'll see a comment left by me with results from a test done on 12 non diabetic humans taking russian tarragon.

by the way slinshot is a great product, nothing but positive reviews! ill put down some links so you could see for yourself!

http://supplementreviews.com/purus-labs/slinshot
http://www.nutraplanet.com/product/purus-labs/slinshot-90-capsules.html
Oh sorry about that, couldn't remember what the name of the active ingredient. My bad
 

uvawahoowa

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oh krap i just saw your comment now, im sorry for my last post!
Good info, I didn't know that was the same thing as Russian tarragon. I'll have to do some further research on that
 

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