Category Archives: Glucose Control

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Phloridzin Effectively Inhibits Glucose Uptake and Traps Advanced Glycation End Products (AGEs)

Phloridzin, also known as Phlorizin, is a glucoside of phloretin, a dihydrochalcone, in the family of bicyclic flavonoids.  It is chemically known as phloretin-2′-β-D-glucopyranoside. 

Phloridzin is primarily found in the skins of apples, in particular, the Malus species.  It is also found in the leaves, bark and seeds of the Malus species.

Phloridzin has been shown to be very effective against glycation and advanced glycation end products (AGEs).  Glycation is considered a main factor in the aging process, which is irreversible when it occurs but can be controlled by diet and supplementation. 

Glycation can form either outside the body through various cooking methods of certain foods and/or inside the body by certain chemical metabolic reactions.  Glycation that occurs outside the body is called exogenous glycation and glycation occuring inside the body is called endogenous glycation. 

Endogenous glycation is the chemical result of the bonding of a sugar molecule with a protein or lipid molecule that produces nonfunctioning and deformed molecules known as advanced glycation end products (AGEs).

Figure 1.  Formation of AGEs  (Source: Glycation and ageing: measurement and treatment from Prime-Journal)

AGEs that stem from a glycation reaction, produces cells that are stiffer and less pliable and more subject to damage and premature aging. When glycated proteins fuse together, this is known as cross-linking. The skin, eyes and heart are particular organs subject to cross-linking.

Exogenous glycation occurs when AGEs are formed by heating proteins and lipids with sugar. Certain forms of cooking can accelerate the exogenous glycation process, such as grilling and frying.

Figure 2. AGEs  (Source: Glycation and ageing: measurement and treatment from Prime-Journal)

AGEs have a range of pathological effects, such as:

  • Increased vascular permeability.
  • Oxidizing LDL.
  • Binding cells—including macrophage, endothelial, and mesangial—to induce the secretion of a variety of cytokines – promoting chronic inflammation.
  • Inhibition of vascular dilation by interfering with nitric oxide.
  • Enhanced oxidative stress – free radicals.

Once an AGE is produced through the endogenous glycation process, it is irreversible. It is therefore important to seek ways to prevent glycation, both endogenously and exogenously.

Mechanism of Phloridzin Against Endogenous Glycation

Phloridzin attacks endogenous glycation in two steps. 

First, phloridzin inhibits glucose uptake by 52%.  1  It inhibits glucose from attaching to the lining cells of the intestine and then blocks the active transport of some, but not all, glucose out of those intestinal lining cells into the bloodstream.  2  3

Second, the glucose that is transported to the bloodstream is responsible for the formation of the dangerous carbonyl molecules that react with proteins and DNA to form AGEs.  4

The formation of these AGEs are prevented by phloridzin by trapping the remaining AGEs that are generated.  This lessens the chain reaction that can occur with AGEs detrimentally reacting with other molecules in the body.  5

In an important study from 2008, researchers found that both phloretin and its glucoside, phloridzin, could efficiently trap certain reactive AGEs called MGO and GO, under physiological conditions.

More than 80% MGO was trapped within 10 min, and 68% GO was trapped within 24 h by phloretin. Phloridzin also had strong trapping efficiency by quenching more than 70% MGO and 60% GO within 24 h. 

This study suggests that dietary flavonoids that have the same A ring structure as phloretin may have the potential to trap reactive dicarbonyl species and therefore inhibit the formation of AGEs.   6  

Berberine exerts a hypoglycemic effect

Berberine is a type of Isoquinoline Alkaloid.

It is found in such plants as Berberis [e.g. Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), Berberis aristata (tree turmeric)], Hydrastis canadensis (goldenseal), Xanthorhiza simplicissima (yellowroot), Phellodendron amurense (Amur cork tree), Coptis chinensis (Chinese goldthread), Tinospora cordifolia, Argemone mexicana (prickly poppy), and Eschscholzia californica (Californian poppy).

Berberine exerts a hypoglycemic effect, but the mechanism remains unknown. In a study at the Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China, the effect of berberine on glucose uptake was characterized in 3T3-L1 adipocytes. It was revealed that berberine stimulated glucose uptake in 3T3-L1 adipocytes in a dose- and time-dependent manner with the maximal effect at 12 hours. Glucose uptake was increased by berberine in 3T3-L1 preadipocytes as well. Berberine-stimulated glucose uptake was additive to that of insulin in 3T3-L1 adipocytes, even at the maximal effective concentrations of both components.

Unlike insulin, the effect of berberine on glucose uptake was insensitive to wortmannin, an inhibitor of phosphatidylinositol 3-kinase, and SB203580, an inhibitor of p38 mitogen-activated protein kinase. Berberine activated extracellular signal-regulated kinase (ERK) 1/2, but PD98059, an ERK kinase inhibitor, only decreased berberine-stimulated glucose uptake by 32%. Berberine did not induce Ser473 phosphorylation of Akt nor enhance insulin-induced phosphorylation of Akt.

Meanwhile, the expression and cellular localization of glucose transporter 4 (GLUT4) were not altered by berberine. Berberine did not increase GLUT1 gene expression. However, genistein, a tyrosine kinase inhibitor, completely blocked berberine-stimulated glucose uptake in 3T3-L1 adipocytes and preadipocytes, suggesting that berberine may induce glucose transport via increasing GLUT1 activity.

In addition, berberine increased adenosine monophosphate-activated protein kinase and acetyl-coenzyme A carboxylase phosphorylation. These findings suggest that berberine increases glucose uptake through a mechanism distinct from insulin, and activated adenosine monophosphate-activated protein kinase seems to be involved in the metabolic effect of berberine. [1]


References:

[1] Zhou, L., et al. Berberine stimulates glucose transport through a mechanism distinct from insulin. Metabolism. 56(3):405-412, 2007.

Zhang Y, Li X, Zou D et al. (July 2008). “Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine”. The Journal of Clinical Endocrinology and Metabolism 93 (7): 2559–65.

Yin J, Xing H, Ye J (May 2008). “Efficacy of berberine in patients with type 2 diabetes mellitus”. Metabolism: Clinical and Experimental 57 (5): 712–7.

Wu LY, Ma ZM, Fan XL et al. (November 2009). “The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells”. Cell Stress & Chaperones 15 (4): 387–94.

Yin J, Gao Z, Liu D, Liu Z, Ye J (January 2008). “Berberine improves glucose metabolism through induction of glycolysis”. American Journal of Physiology. Endocrinology and Metabolism 294 (1): E148–56.

Kong WJ, Zhang H, Song DQ et al. (January 2009). “Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression”. Metabolism 58 (1): 109–19. 


Informational References:

Clinical Applications for Berberine

The Berberine Story Gets Better and Better (Life Enhancement July 2013)

Take This Dye for Diabetes From the ancient Silk Road to the modern nutritional pharmacopeia (By Will Block, Life Enhancement November 2010)


Resources:

Dr. Whittaker – Berberine (500mg)


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Taurine is considered a Wonder Molecule

Taurine’s benefits are very broad and extensive and scientists have described it as a “wonder molecule”.

The often quoted benefits of taurine is that it promotes cardiovascular health, insulin sensitivity, electrolyte balance, hearing function, and immune modulation.

However, it also has the ability to provide protection against reactive carbonyl species and advanced glycation end products (AGE’s).

In a 2004 study at the Department of Biochemistry, Faculty of Science, Annamalai University, Tamil Nadu, India, scientists, Nandhini AT, Thirunavukkarasu V, and Anuradha CV, fed rats a high fructose diet (60% total calories) and then provided a 2% taurine solution for 30 days in order to investigate the antiglycating effect of taurine in high fructose fed rats in vivo and the inhibiting potency of taurine in the process of in vitro glycation.

As a result of the experiment, the contents of glucose, glycated protein, glycosylated haemoglobin and fructosamine were significantly lowered by taurine treatment to high fructose rats. Taurine prevented in vitro glycation and the accumulation of AGEs.

Their conclusion was that these results underline the potential use of taurine as a therapeutic supplement for the prevention of diabetic pathology.


Reference:

Stimulation of glucose utilization and inhibition of protein glycation and AGE products by taurine


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Caiapo Sweet Potato (Ipomoea batatas) Shows Beneficial Effects of Improving Insulin Resistance

The Caiapo sweet potato is a potato variety of the species Ipomoea batatas, and is native to South America, in particular Brazil.  The potato is a white-skinned sweet potato and the dried powder from the potato has been used traditionally as a natural healthy food.

The name Caiapo is dervied from the Kayapo or Caiapó people, a tribe of people that are indigenous to Brazil.   The Caiapó live in the plain islands of the Mato Grosso and Pará in Brazil, south of the Amazon Basin and along Rio Xingu.  1 

Indios Caiapos

There have been a number of studies from 2002 to 2011 that demonstrate the ability of Caiapo (powder) improve glycemic control by reducing insulin resistance.  It is especially beneficial from the conclusion of these studies to reduce fasting blood glucose levels and reduce HbA1c levels.  HbA1c is also known as glycated hemoglobin and is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over prolonged periods.

The four of the most important research studies on the benefits of Caiapo are summarized below:

Study 1  (January 2002)

Recently, it has been shown that caiapo, the extract of white-skinned sweet potato (Ipomoea batatas), improves glycemic control in rodents by reducing insulin resistance. The aim of our study was to assess the effect of caiapo on glucose metabolism and its tolerability and mode of action in male Caucasian type 2 diabetic patients in a randomized, double-blind prospective study in parallel groups controlled with placebo.

This pilot study demonstrates that ingestion of 4 g caiapo/day for 6 weeks reduces fasting blood glucose and total as well as LDL cholesterol in male Caucasian type 2 diabetic patients previously treated by diet alone. The improvement of insulin sensitivity in the FSIGT indicates that caiapo exerts its beneficial effects via reducing insulin resistance. The treatment was well tolerated, with no apparent side effects.

Table 1—Metabolic parameters before (upper line) and after (lower line) treatment with caiapo in the single groups

Placebo Low dose High dose
n 6 6 6
Fasting plasma glucose (mmol/l) 8.2 ± 0.2 8.8 ± 0.4 8.3 ± 0.6
8.4 ± 0.3 8.4 ± 1.1 7.2 ± 0.4*
Fasting plasma insulin (pmol/l) 8.7 ± 1.7 8.3 ± 1.6 13.4 ± 2.5
8.7 ± 1.2 9.0 ± 1.8 13.2 ± 2.5
Total cholesterol (mmol/l) 5.69 ± 0.23 6.05 ± 0.31 4.97 ± 0.21
5.66 ± 0.31 5.68 ± 0.34 4.45 ± 0.18*
LDL cholesterol (mmol/l) 3.72 ± 0.23 4.11 ± 0.28 3.12 ± 0.16
3.78 ± 0.41 3.80 ± 0.28 2.72 ± 0.16*
HDL cholesterol (mmol/l) 1.40 ± 0.10 1.27 ± 0.10 1.16 ± 0.05
1.42 ± 0.16 1.16 ± 0.10 1.11 ± 0.05
Triglycerides (mmol/l) 1.26 ± 0.15 1.45 ± 0.35 1.52 ± 0.19
1.37 ± 0.30 1.61 ± 0.30 1.33 ± 0.13
HbA1c (%) 7.0 ± 0.3 7.3 ± 0.4 7.1 ± 0.3
7.0 ± 0.2 7.3 ± 0.4 6.8 ± 0.3
Blood pressure (mmHg) 134 ± 13 147 ± 18 135 ± 20
130 ± 18 133 ± 19 128 ± 21
BMI (kg/m2) 28.9 ± 0.9 25.5 ± 0.8 28.6 ± 1.3
29.2 ± 0.8 25.8 ± 0.9 28.1 ± 1.5

In conclusion, this pilot study shows beneficial effects of high-dose caiapo on plasma glucose and total as well as LDL cholesterol levels in patients with type 2 diabetes. These effects relate to a decrease in insulin resistance, as also described in rodents, and were observed without affecting body weight or causing side effects. Therefore, the results of this pilot study indicate that caiapo could potentially play a role in the treatment of type 2 diabetes.  2 

Study 2  (February 2004)

To investigate the tolerability, efficacy, and mode of action of Caiapo, an extract of white sweet potatoes, on metabolic control in type 2 diabetic patients.

A total of 61 type 2 diabetic patients treated by diet were given 4 g Caiapo (n = 30; mean age 55.2 ± 2.1 years; BMI 28.0 ± 0.4 kg/m2) or placebo (n = 31; mean age 55.6 ± 1.5 years; BMI 27.6 ± 0.3 kg/m2) once daily for 12 weeks. Each subject underwent a 75-g oral glucose tolerance test (OGTT) at baseline and after 1, 2, and 3 months to assess 2-h glucose levels.

After treatment with Caiapo, HbA1c decreased significantly (P < 0.001) from 7.21 ± 0.15 to 6.68 ± 0.14%, whereas it remained unchanged (P = 0.23) in subjects given placebo (7.04 ± 0.17 vs. 7.10 ± 0.19%). Fasting blood glucose levels decreased (P < 0.001) in the Caiapo group (143.7 ± 1.9 vs. 128.5 ± 1.7 mg/dl) and did not change in the placebo group (144.3 ± 1.9 vs. 138.2 ± 2.1 mg/dl; P = 0.052).

This study confirms the beneficial effects of Caiapo on plasma glucose as well as cholesterol levels in patients with type 2 diabetes. For the first time, the long-term efficacy of Caiapo on glucose control was demonstrated by the observed decrease in HbA1c. Thus, the neutraceutical Caiapo seems to be a useful agent in the treatment of type 2 diabetes.   3 

Figure 1—

Figure 1— Changes in fasting glucose concentration in the two treatment groups during the study period. Asterisks indicate significant differences for Caiapo versus placebo (*P < 0.05; **P < 0.001). See results for additional statistics.

Figure 2—

Figure 2— Changes in glucose concentration measured 2 h after a 75-g oral glucose load in the two treatments during the study period. Asterisks indicate significant differences for Caiapo versus placebo (*P < 0.005; **P < 0.001). See results for additional statistics.

Study 3  (July 2008)

The extract of the white-skinned sweet potato Ipomoea batatas (Caiapo) has been shown to ameliorate glucose control by improving insulin sensitivity in patients with type 2 diabetes mellitus (T2DM). The present study was designed to further evaluate its mode of action on insulin sensitivity over an extended period of time as well as the effects on fibrinogen and other markers of low-grade inflammation.

In this randomized trial, 27 patients with T2DM on diet only received 4 g of Caiapo daily for 5 months; 34 patients placebo. Before and after therapy, insulin sensitivity [oral glucose insulin sensitivity (OGIS), as glucose clearance from oral glucose tolerance test], parameters of diabetes control, lipids, plasma adiponectin, high-sensitivity C-reactive protein (hs-CRP) and fibrinogen were measured.

This study confirms the beneficial effects of Caiapo on glucose and HbA1c control in patients with T2DM after 5 months follow-up. Improvement of insulin sensitivity was accompanied by increased levels of adiponectin and a decrease in fibrinogen. Thus, Caiapo can be considered as natural insulin sensitizer with potential antiatherogenic properties.  4 

Study 4 (March 2011)

Caiapo sweet potato has been found to contain arabinogalactan proteins.  A study from March 2011 examined the effects of an arabinogalactan protein (WSSP-AGP) from Ipomoea batatas L. on hyperglycemia in db/db mice.

An oral glucose tolerance test indicated significantly decreased plasma glucose levels by WSSP-AGP.  Additionally, an insulin tolerance test found improvement in insulin sensitivity due to treatment with WSSP-AGP.

The study’s conclusion suggests that amelioration of insulin resistance by WSSP-AGP causes to lead its hypoglycemic effects.  5 


Informational References:

Fuji-Sangyo Co., Ltd. – Caiapo Potato Powder


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Syzygium cumini: A Tree from the Indian Subcontinent with Multiple Health Benefits

Syzygium cumini, also known as jambul, jambolan, jamblang, or jamun, is an evergreen tropical tree in the flowering plant family Myrtaceae.  Syzygium cumini is native to the Indian Subcontinent and adjoining regions of Southeast Asia. The species ranges across India, Bangladesh, Pakistan, Nepal, Sri Lanka, Malaysia, the Philippines, and Indonesia.  

Syzygium_cumini_Tree_3

Syzygium cumini Tree

The name of the fruit is sometimes mistranslated as blackberry, which is a different fruit in an unrelated family.  In southern Asia, the tree is venerated by Buddhists, and it is commonly planted near Hindu temples because it is considered sacred to Lord Krishna.

The compounds in the tree, including the leaves, fruit, seeds and bark, include:  1

  • Anthocyanins
  • Glucoside
  • Ellagic acid
  • Isoquercetin
  • Kaemferol
  • Myrecetin

The fruit contains:

  • Raffinose
  • Glucose
  • Fructose
  • Citric acid
  • Mallic acid
  • Gallic acid
  • Anthocyanins
  • Delphinidin-3-gentiobioside
  • Malvidin-3-laminaribioside
  • Petunidin-3-gentiobioside
  • Cyanidin diglycoside
  • Petunidin
  • Malvidin

The seeds of the fruit contain:

  • Jambosine
  • Glycoside jambolin

The plant has been considered an anti-diabetic medicinal remedy throughout the Indian and Asian populations.  During the last four decades, numerous folk medicinal reports on the anti-diabetic effects of this plant have been cited in the literature. 

The Table below lists the various folk medicine uses of Syzygium cumini:

Folk medicinal uses of S. cumini (L.) Skeels.
Ethnic group used and their origin Plant part used, mode of preparation, administration and ailments treated References
Local people in southern Brazil Either infusions or decoctions of leaves of jambolan in water at an average concentration of 2.5 g/L and drank it in place of water at a mean daily intake of about 1 liter are used in the treatment of diabetes. [74]
Lakher and Pawi in North east India Infusion of fruit or mixture of powdered bark and fruit is given orally to treat diabetes. [75]
Juice obtained from the seeds is applied externally on sores and ulcers.
Powdered seeds are mixed with sugar are given orally 2–3 times daily in the treatment of dysentery.
The juice of leaves is given orally as antidote in opium poisoning and in centipede bite.
The juice of ripe fruits is stored for 3 days and then is given orally for gastric problems.
The juice obtained from the bark is given orally for the treatment of women with a history of repeated abortion.
Local informants in Maharastra, India Fruit and stem bark are used in the treatment of diabetes, dysentery, increases appetite and to relieve from headache [76]
Nepalese, Lepchas and Bhutias in northeast India Decoction of stem bark is taken orally three times a day for 2–3 weeks to treat diabetes [77]
Native amerindians and Quilombolas in North eastern Brazil Leaves are used in the treatment of diabetes and renal problems. [78]
Kani tribals in Southern India Two teaspoon of juice extracted from the leaf is mixed with honey or cow’s milk and taken orally taken twice a day after food for 3 months to treat diabetes. Fresh fruits are also taken orally to get relief from stomachache and to treat diabetes. [79]
Young leaf is ground into a paste with goat’s milk and taken orally to treat indigestion.
Malayalis in South India Paste of seeds is prepared with the combination of leaves of Momordica charantia and flowers of Cassia auriculata and taken orally once a day for 3 months to treat diabetes. [80]
Traditional medical healers in Madagascar Seeds are taken orally for generations as the centerpiece of an effective therapy for counteracting the slow debilitating impacts of diabetes. [35]
Local population in Andhra Pradesh, India Shade dried seeds are made into powder and taken orally thrice a day in the treatment of diabetes. [81]
Siddis in Karnataka, India The juice obtained from the leaves is mixed with milk and taken orally early in the morning, to treat diabetes. [82]
The juice obtained from the stem bark is mixed with butter milk and taken orally every day before going to bed to treat constipation. The same recipe, when taken early in the morning on an empty stomach, is claimed to stop blood discharge in the faeces.
Rural population in Brazil Leaves of jambolan are taken orally in the treatment of diabetes. [64]
Traditional healers in Brazil


Tea prepared from the infusion or decoction of leaves is taken orally to treat diabetes.


[83]


Tribal people in Maharastra The tender leaves are taken orally to treat jaundice. It was claimed that the eyes, nails and urine turned yellow. The treatment was followed for 2–3 days by adults and children as well. [84]

(Source:  Asian Pac J Trop Biomed. 2012 Mar; 2(3): 240–246.  doi:  10.1016/S2221-1691(12)60050-1)

The fruits, seeds and stem bark of Syzygium cumini possess promising activity against diabetes mellitus which has been confirmed by several experimental and clinical studies and considered its primary health benefit.

There are additional important health benefits of Syzygium cumini that have been studied and published.  They are listed in the Table below:

Health Benefits of Syzygium cumini (Jamun)

SystemConditionBenefitReferences
Gastrointestinal
Gastroprotective
A dose which consisted of 20.0 g tannins/kg rat weight showed significantly lower stomach free radical concentrations. These findings suggest that tannins extracted from S. cumini have gastroprotective and anti-ulcerogenic effects.1
Immunity
Anti-Inflammatory
These observations established the anti-inflammatory effect of S. cuminii seed extract in exudative, proliferative and chronic stages of inflammation along with an anti-pyretic action. Antiinflammatory and related actions of Syzigium cumini seed extract 2
The study concluded that S. cumini exhibits inhibitory role on inflammatory response to histamine, 5-HT and PGE2.3
The present study demonstrated that S. cumini bark extract has a potent anti-inflammatory action against different phases of inflammation without any side effect on gastric mucosa.4
Anti-bacterial and Anti-fungal
The water and methanolic extracts of Syzygium jambolanum seeds were examined for antibacterial and antifungal activity in vitro using the disc diffusion method, minimum inhibitory concentration, minimum bactericidal concentration and minimum fungicidal concentration. 5
The leaf essential oils of Syzygium cumini and Syzygium travancoricum were tested for their antibacterial property. The activity of S. cumini essential oil was found to be good, while that of S. travancoricum was moderate.6
Radioprotective
The radioprotective activity of the hydroalcoholic extract of jamun seeds (SCE) was studied in mice exposed to different doses of gamma radiation. The mice were injected with 0, 5, 10, 20, 40, 60, 80, 100, 120, 140 or 160 mg/kg body weight of SCE, before exposure to 10 Gy of gamma radiation, to select the optimum dose of radiation protection.
The mice treated with 80 mg/kg body weight SCE intraperitoneally before exposure to 6, 7, 8, 9, 10 and 11 Gy of gamma radiation showed reduction in the symptoms of radiation sickness and mortality at all exposure doses and caused a significant increase in the animal survival when compared with the concurrent double distilled water (DDW) + irradiation group. The SCE treatment protected mice against the gastrointestinal as well as bone marrow deaths and the DRF was found to be 1.24.
7
Syzygium cumini Linn. and Eugenia cumini (SCE) provided protection against the radiation-induced bone marrow death in mice treated with 10-60 mg/kg b.wt. of SCE. However, the best protection was obtained for 30 mg/kg b.wt. SCE, where the number of, survivors after 30 days post-irradiation was highest (41.66%) when compared with the other doses of SCE.8
Metabolism
Antioxidant
These data showed that in addition to 5 anthocyanidins, jamun contains appreciable amounts of ellagic acid/ellagitannins, with high antioxidant and antiproliferative activities.9
The leaves, bark and fruits of Terminalia arjuna, Terminalia bellerica, Terminalia chebula and Terminalia muelleri, the leaves and fruits of Phyllanthus emblica, and the seeds of Syzygium cumini were found to have high total phenolic contents (72.0-167.2 mg/g) and high antioxidant activity (69.6-90.6%).10
From the results, using different free radical-scavenging systems, it can be said that the fruit skin of S. cumini have significant antioxidant activity. In each case, lower antioxidant values, in comparison to tea, might be due to drying condition; through which some of antioxidants are presumably degraded. The antioxidant property of the fruit skin may come in part from antioxidant vitamins, phenolics or tannins and/or anthocyanins. Consumption of S. cumini fruit may supply substantial antioxidants which may provide health promoting and disease preventing effects.11
The present study reveals the efficacy of Eugenia jambolana seed kernel in the amelioration of diabetes, which may be attributed to its hypoglycemic property along with its antioxidant potential. The antioxidant effect of Eugenia jambolana seed kernel was also compared with glibenclamide, a standard hypoglycemic drug.12
Diabetes/Blood glucose
The present study reveals the efficacy of Eugenia jambolana seed kernel in the amelioration of diabetes, which may be attributed to its hypoglycemic property along with its antioxidant potential. The antioxidant effect of Eugenia jambolana seed kernel was also compared with glibenclamide, a standard hypoglycemic drug.13
In view of the knowledge summarized here, a successful clinical study should use S. cumini seeds, seed kernels or fruit from India in fairly high doses. Reductions on blood sugar levels by about 30% seem reasonably to be expected. Adverse effects to be expected comprise gastrointestinal disturbances.14
Study shows that S. cumini seed extracts reduce tissue damage in diabetic rat brain.15
Treatment with 400 mg per day of aqueous extracts of Momordica charantia (MC) and Eugenia jambolana (EJ) for 15 days substantially prevented hyperglycemia and hyperinsulinemia induced by a diet high in fructose (63.52+/-2.9 and 66.46+/-2.2 vs. 75.46+/-2.4, respectively).16
The oral antihyperglycemic effect of the water and ethanolic extracts of the fruit-pulp of Eugenia jambolana (EJ) was investigated in alloxan-induced diabetic with fasting blood glucose between 120 and 250 mg/dl as well as severely diabetic rabbits (fasting blood glucose above 250 mg/dl). Water extract was found to be more effective than the ethanolic extract in reducing fasting blood glucose and improving blood glucose in glucose tolerance test.
After treatment of diabetic and severely diabetic rabbits daily once with 25mg/kg, body weight with F-III for 7 and 15 days, respectively, there was fall in fasting blood glucose (38% diabetic; 48% severely diabetic) and improvement in blood glucose during glucose tolerance test (48%) in diabetic rabbits.
17


Resources:

Deep Foods – Frozen Jamun Fruit

Jamun Powder (Syzygium cumini)

Vedic Juices Organic Jamun Indian BlackBerry Juice 1 Liter 12 Packs

Basic Ayurveda – Jamun Juice


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Serum Glucose Control

Nearly four decades ago, Life Extension Foundation emphatically stated that fasting blood glucose should be below 100 (mg/dL). Yet from 1979 to 1997, the medical establishment dictated that one of the criteria for a diagnosis of diabetes was fasting glucose readings of 140 mg/dL or higher on two separate occasions.

In 1997, the medical establishment revised the fasting glucose threshold for a diagnosis of diabetes to 126 mg/dL. In addition, the medical establishment (American Diabetes Association), characterized the so-called impaired fasting glucose threshold level at 110 mg/dL, which was subsequently lowered in 2003 to what Life Extension originally stated, i.e. that no one should have fasting glucose 100 mg/dL or higher.

The problem is that we now know that the optimal fasting glucose ranges are 70-85 mg/dL based upon the totality of the scientific evidence.33

Those with glucose above 85 mg/dL are at increased risk of heart attack.34 This was shown in a study of nearly 2,000 men where fasting blood glucose levels were measured over a 22-year period. The startling results showed that men with fasting glucose over 85 (mg/dL) had a 40% increased risk of death from cardiovascular disease.

The researchers who conducted this study stated “fasting blood glucose values in the upper normal range appears to be an important independent predictor of cardiovascular death in nondiabetic apparently healthy middle-aged men.”34

At a minimum, you want to see your fasting glucose below 86 mg/dL.

Standard laboratory reference ranges allow an upper-limit of fasting glucose of 99 mg/dL. Yet the most effective anti-aging therapy—caloric restriction—lowers fasting glucose levels to the 70-85 mg/dL range.

Recent studies indicate that keeping fasting glucose levels in the range of 70-85 mg/dL and not allowing after-meal glucose levels to spike higher than 40 mg/dL over your fasting value, favorably influences our longevity genes.72

When after-meal glucose levels surge above 140 mg/dL, risks of virtually all degenerative diseases increase.

Remember that you should strive for fasting glucose levels of no greater than 85 mg/dL (optimal range: 70-85 mg/dL). In response to eating, your blood glucose reading should increase no more than 40 mg/dL above your fasting value. This means if your fasting glucose is 80, your after-meal glucose should be no higher than 120 mg/dL.

Source: Life Extension – Glucose: The Silent Killer


References

33. McGlothin, P, Averill M. Glucose Control: The Sweet Spot in Longevity. The CR Way: Using the Secrets of Calorie Restriction for a Longer, Healthier Life. NY: HarperCollins; 2008:57-78.

34. Bjornholt JV, Erikssen G, Aaser E, et al. Fasting blood glucose: an underestimated risk factor for cardiovascular death. Results from a 22-year follow-up of healthy nondiabetic men. Diabetes Care. 1999 Jan;22(1):45-9.

72. Available at: http://www.livingthecrway.com/…/High_Glucose_after_Meals_is…. Accessed August 2, 2010.

73. Available at: http://www.idf.org/webdata/docs/Guideline_PMG_final.pdf. Accessed July 29, 2010.


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Higher glucose levels associated with lower memory and reduced hippocampal microstructure

A study published in the Journal of the American Academy of Neurology indicated that chronically higher blood glucose levels exert a negative influence on cognition, possibly mediated by structural changes in learning-relevant brain areas.

Read the full published study:

Higher glucose levels associated with lower memory and reduced hippocampal microstructure,
Lucia Kerti, MA, A. Veronica Witte, PhD, Angela Winkler, MA, Ulrike Grittner, PhD, Dan Rujescu, MD and Agnes Flöel, MD


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Controlling Blood Glucose levels is Critical to Overall Health

Glucose is a simple monosaccharide. It is one of the three dietary monosaccharides, (the other two being fructose and galactose), that is directly absorbed into the bloodstream during the digestion process.

Our body’s primary source of energy is glucose, which is used by the cells via aerobic respiration or anaerobic respiration. When glucose is properly utilized, our cells produce energy efficiently. As cellular sensitivity to insulin diminishes, excess glucose accumulates in our bloodstream.

Excess blood glucose creates an environment in which oxidative and inflammatory fires chronically erupt. Excess glucose in the bloodstream also initiates the glycation process of glucose molecules bonding with protein or lipid molecules that produce nonfunctioning and deformed molecules known as advanced glycation end products (AGE’s). These damaging glycation reactions fuel the fires of chronic inflammation and incite the production of destructive free radicals.

Excess glucose not used for energy production converts to triglycerides that are either stored as unwanted body fat or accumulate in the blood where they contribute to the formation of atherosclerotic plaque.

There exists scientific data that shows that by taking the proper compounds before meals, the surge of glucose into the bloodstream and the subsequent insulin spike can be mitigated.

Blood Glucose Levels

  • Fasting glucose ranges should be 70-85 mg/dL
  • Above 85 mg/dL are at increased risk of heart attack
  • Do not allow after meal glucose levels to spike higher than 40 mg/dL
  • 85 md/dL plus 40 mg/dL equals 125 mg/dL (Maximum limit of post pandrial glucose level)
  • Never exceed 140 mg/dL post pandrial glucose level

Compounds that are thought to control Blood Glucose Levels:

Vitamins

  • Benfotiamine [1]
  • Alpha Lipoic Acid
  • Niacinamide [2]
  • Pinitol (D-Chiro-Inositol) [3]
  • Biotin [4]

Amino Acids

  • L-Glutamine [5]
  • L-Carnosine
  • Acetyl-l-carnitine

Minerals

  • Vandium
  • Chromium (Polynicotinate form) [6]

Herbs/Foods

  • Cinnamon [7]
  • Berberine [8]
  • Touchi Extract
  • Banaba Leaf [9]
  • Mulberry Extract (Moranoline (Morus Alba leaf)) [10]
  • Gymnema Sylvestre [11]
  • American Ginseng [12]
  • Bitter Melon [13]
  • White Kidney Bean extract (phaseolus vulgaris) [14]
  • Rutin [15]
  • Coffee Berry Extract (chlorogenic acid and caffeic acid)

References:

[1] Hammes, H. P., et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nature Medicine. 9(3):294-299, 2003.

[2] Obrosova, I. G., et al. [Hypoglycemic effect of nicotinamide in diabetes mellitus.] Farmakol Toksikol. 50(2):113-115, 1987.

[3] Bates, S. H., et al. Insulin-like effect of pinitol. British Journal of Pharmacology. 130:1944-1948, 2000.

[4] Koutsikos, D., et al. Oral glucose tolerance test after high-dose i.v. biotin administration in normoglucemic hemodialysis patients. Ren Fail. 18(1):131-137, 1996.

[5] Opara, E. C., et al. L-glutamine supplementation of a high fat diet reduces body weight and attenuates hyperglycemia and hyperinsulinemia in C57BL/6J mice. Journal of Nutrition. 126(1):273-279, 1996.

[6] Preuss, H. G., et al. Chromium update: examining recent literature 1997-1998. Curr Opin Clin Nutr Metab Care. 1:509-512, 1998.

Ravina, A., et al. Reversal of corticosteroid-induced diabetes mellitus with supplemental chromium. Diabetic Medicine. 16(2):164-167, 1999.

Anderson, R. A., et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes. 46:1786-1791, 1997

[7] Hlebowicz, J., et al. Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects. American Journal of Clinical Nutrition. 85(6):1552-1556, 2007.

[8] Zhou, L., et al. Berberine stimulates glucose transport through a mechanism distinct from insulin. Metabolism. 56(3):405-412, 2007.

[9] Klein, G., et al. Antidiabetes and anti-obesity activity of Lagerstroemia speciosa. Evid Based Complement Alternat Med. 4(4):401-407, 2007

[10] Miyahara, C., et al. Inhibitory effects of mulberry leaf extract on postprandial hyperglycemia in normal rats. J Nutr Sci Vitaminol (Tokyo). 50(3):161-164, 2004.

[11] Shimizu, K., et al. Suppression of glucose absorption by some fractions extracted from Gymnema sylvestre leaves. J Vet Med Sci. 59(4):245-251, 1997.

[12] Vuksan, V., et al. American ginseng (Panax quinquefolius L.) attenuates postprandial glycemia in a time-dependent but not dose-dependent manner in healthy individuals. American Journal of Clinical Nutrition. 73(4):753-758, 2001.

[13] Chaturvedi, P., et al. Momordica charantia maintains normal glucose levels and lipid profiles and prevents oxidative stress in diabetic rats subjected to chronic sucrose load. J Med Food.13(3):520-527, 2010.

[14] Tormo, M. A., et al. Hypoglycaemic and anorexigenic activities of an alpha-amylase inhibitor from white kidney beans (Phaseolus vulgaris) in Wistar rats. Br J Nutr. 92(5):785-790, 2004.

[15] Stanley Mainzen Prince, P., et al. Rutin improves glucose homeostasis in streptozotocin diabetic tissues by altering glycolytic and gluconeogenic enzymes. J Biochem Mol Toxicol. 20(2):96-102, 2006.


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