Pursuing optimum health through self-assessment and dispelling misconceptions about nutrition and medicine along the way. We simply can’t know how unfavorable our postprandial glucose levels are unless we check.
And while optimal health is not about fixating on weight—it’s about measuring truly influential parameters like blood glucose, lipid subfractions, and cardiac plaque—nothing will help you lose weight as effectively as understanding how your meals are affecting your blood glucose levels.
Target of this study: Can meal-skipping and nutrient composition of a meal affect postprandial blood glucose levels from a subsequent meal?Dieser Beitrag steht nur registrierten Benutzern mit Berufsverifizierung zur VerfA?gung.
Science, Technology and Medicine open access publisher.Publish, read and share novel research. Glucose Tolerance Factor – Insulin Mimeticand Potentiating Agent – A Source for a Novel Anti Diabetic MedicationNitsa Mirsky[1] Department of Biology, University of Haifa at Oranim, Tivon, Israel1.
P Zhang, X Zhang, J Brown, D Vistisen, R Sicree, J Shaw, G Nichols, 2010Global healthcare expenditure on diabetes for 2010 and 2030 Diab. Orange’s starting glucose level was different between the two meals (as is typical when comparing fasting glucose levels that are days apart), I plotted the graph to show the change in blood glucose from its starting point. Orange’s high-carb meal elevated his blood glucose over his starting point, but what are the absolute values? And we don’t have to think of ourselves as diabetic in order to spend a few days conducting this eye-opening research on ourselves. Orange going to take this lesson to heart and start eating in such a way as to minimize his blood glucose levels? In order to post comments, please make sure JavaScript and Cookies are enabled, and reload the page.
IntroductionDiabetes is the world’s most common metabolic disease and one of the leading causes of morbidity and mortality. S Holdsworth, E Neville, 1990Effects of extracts of high- and low-chromium brewer’s yeast on metabolism of glucose by hepatocytes from rats fed on high- or low-Cr dietsBr. V Mantha, K Prasad, 1995Lipid peroxidation and activity of antioxidant enzymes in diabetic rats.Mol. I Varga, L Szabo, H Witas, 1983The effect of diabetes on the activities of the peroxides metabolizing enzymes. Orange be thinking long and hard about eating more meals that to not elevate his glucose levels?
Starting from a very desirable fasting glucose level of 80, his meal took him from an optimal glucose range into ranges that are toxic to internal organs. A person can read articles about foods that lower or raise the risk of diabetes and can memorize glycemic index tables until her head spins, but nothing can come close to spending a few days with a glucose meter.
The medications currently in use are limited in their potency, have many side effects, and cannot be tolerated by many patients. T Dean, 1987Glucose autoxidation and protein modification: the potential role of autoxidative glycosylation in diabetes.
C Gutteridge, 1984Lipid peroxidation, oxygen radicals, cell damage and antioxidant therapy.
With a little effort and minimal cost, we can measure, not speculate, what we’re doing to ourselves with every single meal. As a result of the global epidemic of diabetes, the need for new diabetes therapies is expected to grow dramatically during the next decade. Reaching these levels day after day, week after week, year after year, slowly destroys our insulin-producing pancreatic beta cells and causes Type 2 diabetes.
An intense research has been conducted to identify new therapeutic targets and pharmacologic compounds that might correct the impaired glucose tolerance.
Materials that mimic insulin action or augment the effect of residual endogenous insulin are likely to be beneficial for both type 1 and 2 diabetic patients. V Arkhipenko, 1982The role of lipid peroxidation in pathogenesis of ischemic damage and antioxidant protection in the heart.
Orange monitored his glucose after a typical meal (a foot-long roast beef sub and diet soda) and compared those measurements to those he took after eating a low-carb meal of feta cheese, avocado, and olive oil a couple of days later. Orange has done, seeing how our typical meals affect our blood glucose, and we change our eating habits to avoid harmful glucose levels, we could make Type 2 diabetes as rare as hen’s teeth. During the recent years many investigators have shown that natural products are a potential source for new drug candidates for many diseases in general, and diabetes in particular. A research aimed at revealing new natural sources to treat diabetes is of high importance.A variety of traditional anti diabetic plants are known in the folk medicine. Although some of them have been studied for their anti diabetic effects, the knowledge on their efficacy and mechanism of action is very limited. The Glucose Tolerance Factor (GTF) is a dietary agent first extracted from Brewer’s yeast [1]. In vitro studies with GTF showed remarkable increase in glucose transport into adipocytes, and cardiomyocytes. An increase in glucose incorporation into glycogen in rat hepatocytes was also found for GTF preparations [2].
Despite the high anti diabetic activity of this natural compound, GTF has not been fully characterized or identified, mainly due to the instability of the purified fractions. Our laboratory succeeded in extraction and partial purification of an active and stable GTF preparation from brewer’s yeast.
We examined GTF effects in animal models for both types of diabetes, and found high and rapid anti diabetic activity. We also examined GTF effects on the cellular level and found high insulin mimetic and insulin potentiating activity for GTF.
Prevalence of diabetes mellitus Diabetes is the world’s most common metabolic disease and one of the leading causes of morbidity and mortality.
According to WHO (World Health Organization) report [3], 346 million people worldwide are diabetic. The number is expected to grow to 438 million until 2030 [8% of the world population!) [4]. Diabetes imposes an increasing economic burden on national health care systems worldwide [5]. The global health expenditure on diabetes in 2010 was 376$ billion and is expected to grow to 490$ billion by 2030 [6]. Diabetes mellitus and its complications Diabetes mellitus is a complex syndrome involving severe insulin dysfunction along with gross abnormalities in glucose homeostasis and lipid and protein metabolism. The disease is generally divided into two major types: Insulin Dependent Diabetes Mellitus (IDDM, or type 1], and Non Insulin Dependent Diabetes Mellitus (NIDDM, or type 2 DM).
People with diabetes have a 25-fold increase in the risk of blindness, a 20-fold increase in the risk of renal failure, a 20-fold increase in the risk of amputation as a result of gangrene and a 2 to 6-fold increase in the risk of coronary heart disease and ischemic brain damage. Diabetes mellitus and oxidative stress Oxidative stress and non enzymatic glycation play a major role in the pathogenesis of diabetes mellitus [7, 8]. During diabetes, persistent high concentrations of blood glucose increase the production of oxygen free radicals – OFRs. Lipid peroxide levels, and especially oxidized LDL, are significantly higher in diabetic patients than in healthy individuals. These Major changes in lipid metabolism cause lipid peroxidation in plasma and cellular membranes which lead to micro and macro vascular pathologies [15]. The natural protective system of antioxidant enzymes like superoxide dismutase, glutathione peroxidase and catalase that provides the detoxification steps for the oxidative products, cannot overcome massive production of free radicals to prevent oxidative damage. It was shown that the activity of the antioxidant systems is decreased in diabetic patients. Diabetes mellitus and aldose reductase The reduction of glucose by the aldose reductase (AR) catalyzed polyol pathway has been linked to the development of secondary diabetic complications like cataract, nephropathy, retinopathy and neuropathy. Accumulation of sorbitol in the organs, due to AR-catalyzed reduction of glucose, causes osmotic swelling resulting in ionic imbalance and protein insolubilization leading to diabetes complications.
Although treatment with AR inhibitors has been shown to prevent tissue injury in animal models of diabetes, the clinical efficacy of these drugs remains to be established. Treatment of diabetes mellitusDaily injections of insulin are the only treatment for type 1 diabetes.

The treatment for type 2 ranges from diet, to classical oral drugs (Sulfonyl urea and biguanides), and to Thiazolidinediones and the new GLP1 analogues. Although the pathogenesis of diabetes and its long-term complications are well known, optimal treatment remains elusive. Only half of the patients achieve the recommended hemoglobin A1c target using conventional treatment [21]. As a result of the global epidemic of diabetes, the need for new diabetes therapies is expected to grow dramatically during the next years. Pharmaceutical research conducted over the past decades has shown that natural sources like herbs, medicinal plants and yeast extract, are potential sources for new drug candidates for many diseases in general [23], and diabetes in particular [24]. Anti diabetic medicinal plantsSeveral reviews published in recent years screen many plant sources with anti-diabetic properties [24, 25, 26, 27, 28, 29].
Garlic has been reported to possess a variety of medicinal properties including hypoglycemic, hypocholesterolemic and hypolipidemic activities [32]. Raw garlic extract reversed proteinuria in diabetic rats in addition to reducing blood glucose, cholesterol and triglyceride in diabetic rats [33]. Silybum Extract (Silybum Marianum) increases the cellular sensitivity to insulin and thus reduces blood glucose total cholesterol and LDL levels in diabetic patients [34]. Bitter cucumber plant fruit (Mamordica Charantia) reduced blood glucose in patients with type 1 diabetes [35]. Studies show that the consumption of one and a half gram dry powder of green tea, improved the metabolism of blood sugar in diabetic patients [36]. Ginkgo biloba plant is capable of lowering glucose, fat, and lipid peroxide in diabetic patients [37]. The ethanolic extract of Allium porrum leaves had hypoglycemic effects on diabetic animals probably through the increase of insulin release [38].
Some nutritional factors, such as polyphenols, counteract insulin resistance and therefore may be beneficial for patients with type 2 diabetes mellitus through their insulin-potentiating, antioxidant, and anti-inflammatory properties. The common cinnamon (CN) has a long history of use as a spice, preservative, and pharmacological agent; CN is also a source of polyphenols. Several studies demonstrated that in animals and humans, CN and aqueous extracts of cinnamon improved the level of blood glucose, lipids and insulin, and may be beneficial to counteract the features of insulin resistance, metabolic syndrome, and the onset of type 2 diabetes mellitus [39, 40, 41, 42].
Yeast as a natural source for anti diabetic materialBrewers' yeast is also included among the anti diabetic natural sources [46, 47]. Schwartz and Mertz were the first to discover the natural anti diabetic agent present in yeast and called it "Glucose Tolerance Factor" (GTF) [1]. Glucose Tolerance Factor (GTF) a natural anti diabetic agent The Glucose Tolerance Factor (GTF) is a dietary agent first extracted from Brewer’s yeast [1]. This natural compound reversed the impaired glucose tolerance of diabetic rats [48, 49], and of diabetic patients [50].
GTF can be extracted from several sources, among them: liver [51], black pepper, and kidneys.
Addition of partially purified GTF to the diet of glucose intolerant rats rapidly returned them to normal [56]. Doisy and his group found an improvement in glucose tolerance in elderly people who were treated for two months with GTF. Offenbacher and Pi Sunyer [46], examined 24 elderly subjects, who were fed daily for 8 weeks with brewers’ yeast as a sorce for GTF. They found a considerable improvement in glucose tolerance and insulin sensitivity, and a reduction of total lipids in these patients. Grant and McMullen [50] treated 37 type 2 diabetics for 7 weeks, in a double blind study, with either brewers’ yeast as a source of GTF, or placebo. Supplementation of brewers’ yeast significantly decreased HbA1c and increased HDL cholesterol in the treated group. Elwood [58] supplemented 11 normolipidemic and 16 hyperlipidemic subjects with brewers’ yeast.
They found that total circulating cholesterol was significantly reduced and the HDL levels were significantly increased in both the normo and hyperlipidemic subjects supplemented with brewers’ yeast.
Riales [59] reported that human subjects receiving 7g of brewers’ yeast for 6 weeks had a significant decrease in serum LDL and an increase in HDL cholesterol. In vitro studies with partially purified preparations of GTF, showed stimulation of glucose metabolism in several tissues. GTF potentiated glucose oxidation to CO2 in adipose tissue [54, 60], or adipocytes [53, 61]. In those studies the enhancement was shown only in the presence of insulin, and the stimulation of CO2 production by GTF in the absence of insulin was negligible [53, 54, 60, 61].
In contrast to the findings above, showing GTF activity only in the presence of insulin, other groups found an increase of glucose metabolism by adding GTF in the absence of insulin. Tokuda et al, [62] examined GTF obtained from yeast extract powder on glucose uptake in adipocytes.
They found a stimulation of glucose uptake (5.6 times greater than the basal level) in the absence of insulin. Our group also showed an increase in glucose transport both to yeast cells [63, 64], and to animal cells [65].Since GTF is supposed to be essential for normal glucose tolerance in mammals, and as muscle tissue consumes a major part of blood glucose in the post prandial state, it is most important to assess the effect of GTF on muscle tissue. Fischer and his group [66] examined the effect of GTF obtained by partial purification of yeast extract, on glucose transport in isolated cardiomyocytes. They found that GTF samples increased the rate of glucose transport in the isolated cells, 2 to 2.5 fold, in the absence of insulin. Hwang et al [67] showed enhancement of 14C -glucose oxidation into CO2 in rat adipocytes by the addition of several fractions extracted from yeast. The authors found only insulin like activity and not insulin potentiating activity for the fractions examined.The exact composition and structure of GTF are still obscure.
Mertz and his group suggested that GTF is probably a small organic molecule comprising one trivalent chromium ion, two molecules of nicotinic acid, and three amino acids: glycine, cystein and glutamic acid [54, 68, 69]. Its molecular weight is estimated to be around 500 daltons [54, 69], It is cationic, soluble in water, and stable in physiological solutions [54, 68].
Several groups who tried to identify the active components present in brewers' yeast, claimed that they are quinoline derivatives [70], or phosphatidylinositol glycans [71].
Other investigators tried to further purify and identify the exact structure and composition of GTF. There is no standard accepted method to isolate GTF, and this fact can probably explain the diversity of the results reported in the literature. In addition, a major problem related to GTF purification, is the instability of the partially purified fractions.
This lability, can partially explain the complexity of the subject, and the fact that in spite of the long time since the material was discovered, its exact composition and structure have not been determined.Tuman [48] who presented the activity of GTF and several synthetic complexes on lowering blood glucose found that in 10 days both the natural compound and the synthetic complexes lost their activity. Mertz reported that highly purified preparations of GTF from yeast or pork kidney tend to be unstable, and lost their activity very quickly [52]. Yamamoto [51] found that GTF like activity of the purified LMCr (low molecular weight chromium binding substance) reduced gradually, and finally there could not be detected any activity. We can explain the instability of the purified fractions of GTF by a loss of a co-factor(s) which is probably responsible for the stability of the complex.Most of the groups who tried to purify GTF from brewers' yeast agree that the GTF is a cationic compound. Only several researchers claimed that the GTF is an anionic compound: Votava and his group [72] reported that GTF is an anionic chromium complex of molecular weight 400-600, containing at least six amino acids.
Since the authors measured only the absorption of the complex by rats, and no biological activity assay was done on it, it is hard to compare Votava’s compound to other extracts exhibiting GTF activity.A low molecular weight chromium binding substance (LMCr), was isolated from mouse or rabbit liver and bovine colostrum by Yamamoto and his group [51, 73]. LMCr appears as anionic organic Cr compound, with a relative molecular mass of 1500 daltons. The purified LMCr enhanced glucose conversion to CO2 in rat epididymal adipocytes in the presence of insulin.
The rate of glucose incorporation into lipid was stimulated by 30-40% with insulin, or by 15-23% without insulin [51]. Yamamoto and his colleagues were not able to detect nicotinic acid in the extract of LMCr, but some UV absorption was present [73]. Urumow & Wieland [74], suggested that GTF activity in stimulating 14C-glucose oxidation is attributable to the combined action of certain amino acids (aspartate, cystein) and nucleosides (adenosine).

Fischer [66] came to a conclusion that GTF activity is attributed to the presence of alanine. Hwang and his group [70] suggested that the GTF obtained was a quinoline derivative, which easily binds chromium.While many research groups in the past agreed with the concept suggested by Mertz that GTF contains chromium [51, 55, 73, 75], accumulating data during the years indicates that there is no chromium present in the GTF preparation. Haylock and his group, who tried to purify and identify GTF for many years, did not find a correlation between chromium content and the biologic activity. They came to the conclusion that: "GTF from brewers' yeast can no longer be regarded as a chromium complex" [76]. Stearns [78] summarized the purification research that had been done on GTF and discussed the relation of the active component to chromium. Stearns also investigated the issue of the essentiality of chromium to human health, and found that "no chromium-containing glucose tolerance factor has been characterized, the purpose of the low-molecular-weight chromium-binding protein is questionable, and no direct interaction between chromium and insulin has been found" [79]. Moreover, she criticized the dietary supplementation of chromium: "Chromium+3 may act clinically by decreasing the iron stores that are linked to diabetes and heart disease.
Eddens and his colleagues [47], isolated three separate fractions by eluting yeast extract from C18 column and found diverse activities in increasing glucose metabolism and inhibiting lipolysis for the different fractions, not connected to their chromium content. We used several separation techniques including membranes with different molecular cut off, ion exchange columns and reversed phase HPLC. It was found to be very stable: it is stable to high and low pH and it keeps its activity up to 12 months in 4°C. This finding enables an oral treatment with GTF, in contrast to insulin, which is a protein and has to be injected [49, 80, 81]. In the following paragraphs we shall present several of our findings on GTF both in vivo and in vitro. We examined GTF effects in animal models for both types of diabetes, and found high and rapid anti diabetic, hypolipidemic and antioxidant activity. We also found a remarkable reduction in the complications of diabetes: nephropathy and retinopathy, by treating the diabetic animals with oral doses of GTF [81]. In vitro studies done in our laboratory showed insulin mimetic and insulin potentiating activity for GTF [65].9. GTF decreases blood glucose in diabetic rat modelsA single oral dose of GTF, orally administered to both types of diabetic animals, decreased immediately and remarkably glucose and lipid levels in their blood [49, 80]. Glucose reduction appeared immediately after the administration of GTF, reached a maximum within 2 hours, and lasted for several hours.
When GTF was administered in concert with marginal insulin doses, the reduction in blood glucose was much higher than for each agent alone, demonstrating a synergy between GTF and insulin [80].
Insulin secretion in response to glucose stimulation did not change significantly in GTF treated hyp-CDs rats (From Wexler-Zangen et al, [65], indicating that the glucose lowering effect of GTF is not related to stimulation of insulin secretion.
GTF reduces postprandial blood glucose concentration in diabetic ratsPost prandial (PP) blood glucose level is very high in both hyp-CDs and STZ diabetic rats. In the vehicle treated hyp-CDs and STZ rats, the markedly elevated BG concentrations remained high for more than 120 min (Figs 2A and B). GTF decreases tri glyceride and LDL cholesterol and increases HDL cholesterolA remarkable decrease in triglyceride level was observed in diabetic animals administered with 5 daily oral doses of GTF (Figure 3). The treatment with GTF also remarkably decreased the level of LDL cholesterol (Figure 4A), and increased the level of HDL cholesterol (Figure 4B), (Ampel et al., unpublished data). GTF reduces lipid peroxidation in the plasma, both in vivo and in vitroGTF can inhibit the deleterious elevation in lipid peroxides induced by diabetes.
The animals were killed and the levels of lipid peroxidation products - malondialdehyde (measured as TBARS – thiobarbituric acid reactive substances), in healthy, diabetic and diabetic rats treated with GTF were determined. Figure 5 demonstrates the level of lipid peroxidation products detected in the plasma of healthy, diabetic, and diabetic rats treated with GTF, showing a major decrease in the level of plasma peroxides in diabetic animals treated with GTF. The value of lipid peroxides in untreated diabetic rats was significantly higher than the value detected for healthy animals. The level of lipid peroxides in the hearts of diabetic rats treated with 5 oral doses of GTF was very low - a higher effect seen for the higher dose of GTF, similar to the level found in healthy animals. A remarkable decrease in lipid peroxidation level is shown also in kidneys removed from diabetic rats treated with GTF (Figure 7). Peroxide values found in the animals treated with GTF were very similar to those found in healthy controls.
GTF decreases aldose reductase activityElevated activity of aldose reductase (AR) in the organs is one of the events occurring in hyperglycemic conditions. We measured aldose reductase activity in the hearts of healthy, diabetic and diabetic treated with GTF (Figure 8).
AR activity in the hearts of diabetic rats was much higher than that found in healthy rats. Products of lipid peroxidation were measured in the presence (induced) and absence (non-induced) of FeSO4. Decreased urine volume and urine protein in diabetic rats treated with GTFWe measured the urine volume and urine protein of healthy, diabetic, and diabetic rats treated for two weeks with oral doses of GTF. The group of diabetic animals treated with GTF received daily doses of GTF mixed in their food immediately with the induction of diabetes. GFAP expression in healthy, diabetic and Diabetic rats treated with GTF Glial Fibrillary Acidic Protein (GFAP) is normally expressed in retinal astrocytes. Under pathologic conditions like hyperglycemia or ischemia, GFAP can be detected in other retina's areas like Muller cells layer. A prevention of the damage could be detected in retinas isolated from diabetic animals treated for two weeks with GTF, where the activity of the pump is similar to the activity shown for healthy controls. Mechanism of action of GTF: Insulin mimetic activity Binding of insulin to its receptor initiates a cascade of phosphorylations of several substrates, including insulin receptor substrate (IRS) proteins. IRS-1 is widely expressed in insulin-sensitive tissues, and it transmits the signal from insulin receptor to biological endpoints, such as glucose transport, protein, lipid, and glycogen synthesis. Studies done in our laboratory on L6 myoblasts and 3T3-L1 adipocytes presented a marked increase in 2-deoxy-glucose [2-DG) uptake induced by GTF, in a rate similar to insulin, indicating a high positive effect on glucose uptake (Figure 13) (From Weksler-Zangen et al., [65]. Cells were dissolved in 1N NaOH, and aliquots were taken for scintillation counting and protein determination. We also found that the increased glucose transport induced by GTF is dose dependent (Weksler-Zangen et al., [65]. A similar synergy between GTF and insulin that was demonstrated in diabetic animals in vivo was also found in vitro: The increase in 2-DG transport detected for the combination of GTF and insulin was much higher than for each agent alone. The rate of 2-DG transport found for the combined treatment exceeded the sum of the two separate treatments, indicating a synergy between GTF and insulin (Weksler-Zangen et al., [65].
We also found increased phosphorylation of key proteins along insulin signaling pathway, like IRS1, AKT, ccbl and MAPK, by the addition of GTF to the medium (Figures 14-16). However, we did not find any augmented phosphorylation of the insulin receptor following GTF addition, indicating a possible "by pass" of the insulin receptor by GTF. Cells were lysed and western blot analysis was performed with antibodies for phosphotyrosine followed by stripping and reblotting with antibodies for total IRS1 as a loading control. Cells were lysed and western blot analysis was performed with antibodies for phospho-Akt followed by stripping and reblotting with antibodies for total Akt as a loading control.
ConclusionsIn a search for new and effective medications for diabetes mellitus, there is a growing interest in natural derived hypoglycemic agents such as medicinal plants, herbs, and yeast. The Glucose Tolerance Factor (GTF), which is an active anti diabetic material extracted from yeast, is presented in the current manuscript.GTF effectively decreased the elevated blood glucose in diabetic animals and humans. It also decreased triglycerides and LDL cholestrerol and increased HDL cholesterol in diabetic subjects.
GTF treatment also prevented diabetes complications like nephropathy and retinopathy.Not being a protein, GTF can be taken orally.
These results demonstrate GTF as a potential natural source for a novel oral anti diabetic drug in the future.

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