Denise released research years ago showing that her method is able to reverse Type 1 Diabetes in mice, which was later verified by independent labs.

She is finally beginning her human trials! Another year, and we should see some results.

The great part about Denise’s research is that she is looking at curing the disease in people who have had it for many years. Most new trials that are happening right now are for newly diagnosed Type 1 Diabetics who still have some pancreatic function, as opposed to someone with long standing Diabetes.

It is great to have hope! In the meantime, I will stay healthy with my supplement regime and hope for the best.

The findings are not too suprising, as moderate exercise is of course beneficial to Diabetics, but it is good to see the research.

The BBC has a good writeup on this recent study.

The study was done in Manchester at the St. Mary’s Hospital for Women and Children. The effect was dose-dependent and should certainly be of interest to anyone with young children who are at risk for developing Type 1 Diabetes.

The BBC has a good writeup on the piece- Vitamin D “Cuts Risk of Diabetes”.

I have an extensive review of the research surrounding Chromium, but I have not done any research on Magnesium yet. It appears that studies are associating low levels of Magnesium with insulin utilization problems and Type 2 Diabetes. Read the study - Serum zinc, chromium and magnesium levels in Type 2 diabetes, published in 2006.

The complete article I found is here.

Magnesium appears to be an important mineral and I am going to do more research into this mineral for Diabetes.

The study  is in the February issue of Diabetes Care entitled - Salsalate Improves Glycemia and Inflammatory Parameters in Obese Young Adults. The study examined inflammatory markers such as C-peptide levels and glucose levels in 20 obese patients for a month.

The results look pretty clear- a reduction in the fasting glucose tolerance test, reduced C-peptide levels, and improved insulin sensitivity. Further research is neccessary to see how helpful this drug could be in the long term, but this study certainly looks promising.

It has been found that the poly oxovanadium complex exhibits potent antidiabetic activity in diabetes type I and type 2 in mice. (Ref 2)

Studies indicate that the oral vanadyl acetyl acetonate is well tolerated and benefits diabetic osteopathy of rats and improves diabetes related bone disorders particularly by improving the diabetic state. (Ref 3)

Vanadium is a well known anti-diabetic agent which mimics most of the actions of insulin on mature adipocytes.  Studies (Ref 4) show a new dimension in vanadium treatment for diabetes due to its novel role in adipogenensis.

Bis oxovanadium (IV) is a new orally active anti-diabetic organic vanadium complex and it has anti-diabetic and insulin-sensitizing effects in diabetic rats, exhibiting the potential to be developed as a new therapeutic agent for type 2 diabetes. (Ref 5)  

Bis oxovanadium (IV) is a safe and potent agent for diabetes treatment because it is able to improve carbohydrate metabolism and to reduce oxidative stress. (Ref 6)

Vanadyl sulfate and taurine are two promising agents in the treatment of diabetes related to their antihyperglycemic, antihyperlipemic, and hyperinsulinemic effects.  (Ref 7)

An oxovanadium complex has been tested for bioactivity as an insulin enhancing agent and results showed that the complex at specific doses could lower the blood glucose level in STZ-diabetic rats and improve the response to an oral glucose challenge. (Ref

Oxovanadium is proposed to be an orally active complex for treating type I diabetes and type 2 diabetes in animals. (Ref 9)

A review has been done regarding vanadium’s glucose-enhancing potential, its biodistribution, and biomolecular transformation and its mechanism of action in diabetes treatment. (Ref 10)

The diabetes-associated biochemical and morphological alterations in Golgi complexes were investigated and results showed that sodium metavandate affected diabetic rat liver Golgi complexes. (Ref 11)

Insulin-mimetic vanadyl-poly complex is proposed as a novel drug delivery system for treating type 1 diabetic animals and results showed improvement in diabetes as seen by results on oral glucose tolerance test, HbA(1c) levels, and blood pressure. (Ref 13, 14)

Research data indicate immense hypoglycemic activity and reduced toxicity of oxovanadium complex. (Ref 15)

Treatment with Vanadium, a representative of class of anti-diabetic compounds alleviates hyperglycemia and hyperlipidemia.  Oral administration of vanadium compounds in animal models and humans does not cause clinical symptoms of hypoglycemia, a common problem for diabetic patients with insulin treatment. (Ref 16)

Studies have showed that vanadyl sulfate trihydrate can inhibit c AMP dependent protein kinase. (Ref 17) 

Among several metals, Vanadium has emerged as an extremely potent agent with insulin-like properties.  These insulin-like properties have been demonstrated in isolated cells, tissues, different animal models of type 1 an dtype2 diabetes as well as on a limited number of human subjects.  Insulin signal mimicry is suggested as a mechanism for the insulin-like effects of Vanadium.

1. Effect of vanadate on gene expression of the insulin signaling pathway in skeletal muscle of streptozotocin-induced diabetic rats. J Biol Inorg Chem. 2007 Nov; 12(8):1265-73. Epub 2007 Sep 14.
   

2. Amelioration of Hyperglycemia and Metabolic Syndromes in Type 2 Diabetic KKA(y) Mice by Poly (gamma-glutamic acid) oxovanadium (IV) Complex. ChemMedChem. 2007 Nov;2(11):1607-12.
   

3. Effects on the bones of vanadyl acetylacetonate by oral administration: a comparison study in diabetic rats. J Bone Miner Metab. 2007; 25(5):293-301. Epub 2007 Aug 25.
   

4. Adipogenic action of vanadium: a new dimension in treating diabetes. Biometals. 2007 Aug 2; [Epub ahead of print]
   

5. Effects of bis(alpha-furancarboxylato)oxovanadium(IV) on glucose metabolism in fat-fed/streptozotocin-diabetic rats. Eur J Pharmacol. 2007 Oct 31; 572(2-3):213-9. Epub 2007 Jun 19.
   

6. Bis (quercetinato) oxovanadium IV Reverses Metabolic Changes in Streptozotocin-Induced Diabetic Mice. Rev Diabet Stud. 2007 Spring;4(1):33-43. Epub 2007 May 10.
   

7. Vanadyl sulfate, taurine, and combined vanadyl sulfate and taurine treatments in diabetic rats: effects on the oxidative and antioxidative systems. Arch Med Res. 2007 Apr; 38(3):276-83. Epub 2007 Jan 22.
   

8. In vivo insulin-mimetic activity of [N, N’-1, 3-propyl-bis (salicyladimine)]oxovanadium(IV). Eur J Med Chem. 2007 Jun; 42(6):817-22. Epub 2007 Jan 12.
   

9. Improvement of hyperglycaemia and metabolic syndromes in type 2 diabetic KKAy mice by oral treatment with [meso-tetrakis (4-sulfonatophenyl) porphyrinato] oxovanadium (IV) (4- ) complex. J Pharm Pharmacol. 2007 Mar; 59(3):437-44. 
   

10. Vanadium in diabetes: 100 years from Phase 0 to Phase I. J Inorg Biochem. 2006 Dec; 100(12):1925-35. Epub 2006 Sep 7.
    

11. Sodium metavanadate affected control and streptozotocin-diabetic rat liver golgi complexes. Pol J Pathol. 2006; 57(2):91-7. 
    

12. Follow-up studies on glycosylated flavonoids and their complexes with vanadium: their anti-hyperglycemic potential role in diabetes. Chem Biol Interact. 2006 Nov 7; 163(3):177-91. Epub 2006 Aug 12.
    

13. A novel drug delivery system for type 1 diabetes: insulin-mimetic vanadyl-poly (gamma-glutamic acid) complex. J Inorg Biochem. 2006 Sep; 100(9):1535-46. Epub 2006 May 24.
    

14. Bis (allixinato) oxovanadium (IV) complex is a potent antidiabetic agent: studies on structure-activity relationship for a series of hydroxypyrone-vanadium complexes. J Med Chem. 2006 Jun 1; 49(11):3251-6.
    

15. Reduction of oxidative stress induced vanadium toxicity by complexing with a flavonoid, quercetin: a pragmatic therapeutic approach for diabetes. Biometals. 2006 Dec; 19(6):685-93. Epub 2006 May 16.
    

16. Diabetes-altered gene expression in rat skeletal muscle corrected by oral administration of vanadyl sulfate. Physiol Genomics. 2006 Aug 16; 26(3):192-201. Epub 2006 May 9.
    

17. Inhibition of cyclic AMP dependent protein kinase by vanadyl sulfate. J Biol Inorg Chem. 2006 Apr; 11(3):379-88. Epub 2006 Feb 28.
    

18. Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium. Cell Biochem Biophys. 2006; 44(1):73-81.

The research study in reference 2 suggests that chromium supplementation can lower the risk of vascular inflammation in diabetes.  Results indicated that metabolic disorders such as type2 diabetes mellitus, hypertension, dyslipidemia and obesity are associated with variations in serum levels and poor delivery of certain mineral elements like magnesium, copper, zinc, chromium and nickel. (Ref 3)

Research study showed that chromium picolinate has marked beneficial effects against macrovascular complications and its potential role in diabetes management. (Ref 4)

Dyslipidemia, often found in type 2 diabetes mellitus patients, plays an important role in the process of cardiometabolic syndrome.  A randomized, double-blind, placebo-controlled trial was done to evaluate the effect of chromium picolinate and biotin on lipid and lipoprotein levels.  Data suggests that intervention with chromium picolinate biotin improves cardiometabolic risk factors. (Ref 5, 9)

Chromium yeast supplementation can be considered to improve carbohydrate and lipid metabolism amongst human patients featuring type 2 diabetes mellitus. (Ref 6)

Another research suggests that chromium niacinate supplementation may be useful in reducing vascular inflammation and the risk of CVD in diabetes. (Ref 7)

Chromium supplementation significantly improved glycemia in diabetic patients as per a systemic review of the effect of chromium supplementation on glucose metabolism and lipid levels. (Ref 8)  

Glucose intolerance (type 2 diabetes mellitus) is an important factor that disturbs Chromium metabolism. (Ref 10)

Data supports the safety and therapeutic value of Chromium picolinate for the management of cholesterolemia and hyperglycemia in subjects with diabetes. (Ref 12)

According to a pilot study in diabetes type 2 patients chromium/biotin supplementation may represent an effective adjunctive nutritional therapy to people with poorly controlled diabetes with the potential for improving lipid metabolism. (Ref 13)

Results of study in reference 14 indicated that the effect of decreasing blood sugar by chromium complexes of D-glucosaminic acid was comparable to that of chromium complex currently used worldwide. (Ref 14)

Chromium picolinate supplementation in subjects with type2 diabetes who are taking sulfonylurea agents significantly improves insulin sensitivity and glucose control, and chromium picolinate supplementation significantly attenuated body weight and visceral fat accumulation compared with placebo group. (Ref 15)

Intake of milk powder containing 40 mcg/d of chromium for 16 weeks in subjects with type 2 diabetes mellitus resulted in lowering of FPG, fasting insulin, and improvement of metabolic insulin control in male patients. (Ref 16)

Chromium included early in the complex therapy is beneficial in the reduction of the degree of insulin resistance. (Ref 17)

Data from research study suggest that supplementation of well-controlled type 2 diabetes with chromium enriched yeast is safe and can result in improvements in blood glucose variables and oxidative stress. (Ref 18)

1. Chromium in metabolic and cardiovascular disease. Horm Metab Res. 2007 Oct; 39(10):743-51.

2. Effect of chromium niacinate and chromium picolinate supplementation on lipid peroxidation, TNF-alpha, IL-6, CRP, glycated hemoglobin, triglycerides, and cholesterol levels in blood of streptozotocin-treated diabetic rats. Free Radic Biol Med. 2007 Oct 15; 43(8):1124-31. Epub 2007 May 18.

3. Plasma mineral content in type-2 diabetic patients and their association with the metabolic syndrome. Ann Nutr Metab. 2007; 51(5):402-6. Epub 2007 Sep 11.

4. Effect of chromium on carbohydrate and lipid metabolism in a rat model of type 2 diabetes mellitus: the fat-fed, streptozotocin-treated rat. Metabolism. 2007 Sep; 56(9):1233-40.

5. Combination of chromium and biotin improves coronary risk factors in hypercholesterolemic type 2 diabetes mellitus: a placebo-controlled, double-blind randomized clinical trial. J Cardiometab Syndr. 2007 Spring; 2(2):91-7.

6. Chromium yeast supplementation improves fasting plasma glucose and LDL-cholesterol in streptozotocin-induced diabetic rats. Int J Vitam Nutr Res. 2006 Nov; 76(6):391-7.

7. High glucose and ketosis (acetoacetate) increases, and chromium niacinate decreases, IL-6, IL-8, and MCP-1 secretion and oxidative stress in U937 monocytes. Antioxid Redox Signal. 2007 Oct;9(10):1581-90.

8. Effect of chromium supplementation on glucose metabolism and lipids: a systematic review of randomized controlled trials. Diabetes Care. 2007 Aug; 30(8):2154-63. Epub 2007 May 22.

9. Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. Diabetes Metab Res Rev. 2007 May 16; 24(1):41-51 [Epub ahead of print]

10. Longitudinal hair chromium profiles of elderly subjects with normal glucose tolerance and type 2 diabetes mellitus. Metabolism. 2007 Jan; 56(1):94-104.

11. Chromium picolinate supplementation attenuates body weight gain and increases insulin sensitivity in subjects with type 2 diabetes: response to Martin et al. Diabetes Care. 2006 Dec; 29(12):2764; author reply 2764-5.

12. Clinical studies on chromium picolinate supplementation in diabetes mellitus–a review. Diabetes Technol Ther. 2006 Dec;8(6):677-87.

13. The effect of chromium picolinate and biotin supplementation on glycemic control in poorly controlled patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized trial. Diabetes Technol Ther. 2006 Dec;8(6):636-43.

14. Chromium (III) complexes of D-glucosaminic acid and their effect on decreasing blood sugar in vivo. Arch Pharm (Weinheim). 2006 Sep; 339(9):527-30.

15. Chromium picolinate supplementation attenuates body weight gain and increases insulin sensitivity in subjects with type 2 diabetes. Diabetes Care. 2006 Aug; 29(8):1826-32.

16. The influence of chromium chloride-containing milk to glycemic control of patients with type 2 diabetes mellitus: a randomized, double-blind, placebo-controlled trial. Metabolism. 2006 Jul; 55(7):923-7.

17. Effect of chromium on the insulin resistance in patients with type II diabetes mellitus. Folia Med (Plovdiv). 2005; 47(3-4):59-62.

18. Influence of chromium-enriched yeast on blood glucose and insulin variables, blood lipids, and markers of oxidative stress in subjects with type 2 diabetes mellitus. Biol Trace Elem Res. 2006 Mar; 109(3):215-30.

Gymnema sylvestre preparations have profound action on modulation of taste, particularly sweet sensations. It is used in treatment of diabetes mellitus and in food additives against obesity and caries. Anti-allergic, antiviral, lipid lowering and other effects have also been reported (ref 6).

Research on crude saponin fraction and five triterpene glycosides derived from methanol extract of leaves of Gymnema sylvestre in diabetic rats indicate that insulin-releasing action of gymnemic acid IV may contribute to the antihyperglycemic effect of leaves of Gymnema sylvestre. Gymnemic acid IV may be an anti-obese and antihyperglycemic pro-drug (ref 7).

Therapeutic potential of Gymnema sylvestre for treatment of non-insulin-dependent diabetes mellitus (NIDDM) has been examined the results confirm the stimulatory effect of Gymnema sylvestre on insulin release and indicate that Gymnema sylvestre acts by increasing cell permeability, rather than stimulating exocytosis by regulated pathways (ref 8).

In ref 12 studies on diabetic patients to study the anti diabetic effect of a leaf extract from Gymnema sylvestre in NIDDM patients showed a significant reduction in blood glucose, glycosylated hemoglobin and glycosylated plasma proteins, and conventional drug dosage could be decreased. Data suggest that the beta cells may be regenerated/repaired in Type 2 diabetic patients on GS4 (Gymnema sylvestre aqueous extract) supplementation. GS4 therapy appears to enhance endogenous insulin, possibly by regeneration / revitalization of residual beta cells in insulin dependent diabetes mellitus (IDDM) as suggested by research in ref 13 and 14.

Effect of Gymnema sylvestre on glucose homeostasis in rats suggested the usefulness of Gymnema sylvestre in the treatment of certain classes of non-insulin-dependent diabetes mellitus.

1. Gymnema sylvestre for Diabetes Mellitus: A Systematic Review.

   J Altern Complement Med. 2007 Nov; 13(9):977-84.

2. Extraction and quantification of gymnemic acids through gymnemagenin from callus cultures of Gymnema sylvestre.

   Phytochem Anal. 2006 Nov; 17(6):409-13.

3. Effect of Dianex, a herbal formulation on experimentally induced diabetes mellitus.

   Phytother Res. 2005 May; 19(5):409-15.

4. Advances in the study on hypoglycemic constituents of Gymnema sylvestre (Retz.)

   Zhong Yao Cai. 2003 Apr; 26(4):305-7. Review. Chinese.

5. Effects of Inula racemosa root and Gymnema sylvestre leaf extracts in the regulation of corticosteroid induced diabetes mellitus: involvement of thyroid hormones.

   Pharmazie. 2003 Jun; 58(6):413-5.

6. An overview on the advances of Gymnema sylvestre: chemistry, pharmacology and patents.

   Pharmazie. 2003 Jan; 58(1):5-12. Review.

7. Antihyperglycemic effects of gymnemic acid IV, a compound derived from Gymnema sylvestre leaves in streptozotocin-diabetic mice.

   J Asian Nat Prod Res. 2000;2(4):321-7.

8. Gymnema sylvestre stimulates insulin release in vitro by increased membrane permeability.

   J Endocrinol. 1999 Nov; 163(2):207-12.

9. Gymnema sylvestre.

   Altern Med Rev. 1999 Feb;4(1):46-7.

10. Medicinal foodstuffs. IX. The inhibitors of glucose absorption from the leaves of Gymnema sylvestre R. BR. (Asclepiadaceae): structures of gymnemosides a and b.Chem Pharm Bull (Tokyo). 1997 Oct; 45(10):1671-6.

11. Effects of seishin-renshi-in and Gymnema sylvestre on insulin resistance in streptozotocin-induced diabetic rats.

    Diabetes Res Clin Pract. 1995 Jul; 29(1):11-7.

12. Antidiabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients.

    J Ethnopharmacol. 1990 Oct; 30(3):295-300.

13. Use of Gymnema sylvestre leaf extract in the control of blood glucose in insulin-dependent diabetes mellitus.

    J Ethnopharmacol. 1990 Oct; 30(3):281-94.

14. Possible regeneration of the islets of Langerhans in streptozotocin-diabetic rats given Gymnema sylvestre leaf extracts.

    J Ethnopharmacol. 1990 Oct; 30(3):265-79.

15. Effect of Gymnema sylvestre, R.Br. on glucose homeostasis in rats.

    Diabetes Res Clin Pract. 1990 May-Jun; 9(2):143-8.

16. Hypoglycaemic activity of an indigenous drug (Gymnema sylvestre, ‘Gurmar’) in normal and diabetic persons.

    Indian J Physiol Pharmacol. 1983 Jul-Sep; 27(3):257-8.

Fenugreek (Trigonella foenum-graecum) seeds have shown to have hypoglycemic and hypocholesterolemic effects on type1 & type2 diabetes mellitus patients and experimental diabetic animals. Supplementation of fenugreek leaves lowers the lipid-profile in diabetes mellitus (ref.15). Supplementation with Fenugreek leaves improves body weight and liver glycogen and has a significant effect of carbohydrate metabolism similar to Glibenclamide (ref. 16). Studies (ref 3) indicate that soluble dietary fraction of fenugreek seeds exerts anti-diabetic effects mediated through inhibition of carbohydrate digestion and absorption, and enhancement of peripheral insulin action.

Fenugreek also corrected the alterations in the distribution of skeletal muscle glucose transporter GLU4 (ref 4). The results of study in ref 1 show enrichment of fenugreek extracts, which has implications for diet-based diabetes management.

Fenugreek and Sodium orthovandate alone or in low dose combination have been shown to effectively control ocular histopathological and biochemical abnormalities associated with diabetic retinopathy (ref 5). Low doses of Vandate and Trigonella in combination was effective in normalization of altered membrane linked functions and GLU4 distribution without any side effects (ref.6,7).

Another study concludes that 2g of a powdered mixture of 3 medicinal plants (bitter gourd, jamun seeds and fenugreek) in raw or cooked form can be successfully used n lowering blood glucose in diabetes (ref.8)

Research suggests that low doses of Na3VO4 in combination with Trigonella seed powder are an efficient antidiabetic agent to control long-term complications of diabetes in tissues such as peripheral nerves (ref. 9).

Fenugreek leaf powder reduces oxidative stress in experimental diabetes. Fenugreek supplementation significantly lowered lipid peroxidation and significantly increased antioxidant system in diabetic rats in research study (ref. 10).

Research studies have noted positive influence of feeding fenugreek seed mucilage and spent turmeric on intestinal and renal disaccharides and thus their beneficial role in diabetes management (ref.11).

The hypoglycemic activity of fenugreek seed extract is mediated through the stimulation of an insulin signaling pathway (ref.12)

Fenugreek seed powder protects against histopathological abnormalities in tissues as well as acts to normalize metabolism which proves its potential as an antidiabetic agent (ref.13).

Fenugreek seeds are rich in protein and contain the unique free amino acid 4-hydoxyisoleucine (4-OH-Ile), which has been characterized as one of the active ingredients for blood glucose control. Potential genotoxicity of fenugreek seed extract was evaluated using FDA recommended tests and it was determined not to be genotoxic (ref.14).

Research studies (ref.2) conclude that Fenugreek extract can lower kidney/body weight ratio, blood glucose, blood lipid levels and improve hemorheological properties in experimental diabetic rats.

1. Improved alpha-amylase and Helicobacter pylori inhibition by fenugreek extracts derived via solid-state bioconversion using Rhizopus oligosporus Asia Pac J Clin Nutr. 2007; 16(3):382-92.
2. Effect of Trigonella foenum-graecum (fenugreek) extract on blood glucose, blood lipid and hemorheological properties in streptozotocin-induced diabetic rats. Asia Pac J Clin Nutr. 2007; 16 Suppl 1:422-6.
3. Soluble dietary fibre fraction of Trigonella foenum-graecum (fenugreek) seed improves glucose homeostasis in animal models of type 1 and type 2 diabetes by delaying carbohydrate digestion and absorption, and enhancing insulin action. Br J Nutr. 2007 Mar; 97(3):514-21.
4. In vivo effect of Trigonella foenum graecum on the expression of pyruvate kinase, phosphoenolpyruvate carboxykinase, and distribution of glucose transporter (GLUT4) in alloxan-diabetic rats. Can J Physiol Pharmacol. 2006 Jun;84(6):647-54.
5. Long-term effect of Trigonella foenum graecum and its combination with sodium orthovanadate in preventing histopathological and biochemical abnormalities in diabetic rat ocular tissues. Mol Cell Biochem. 2006 Sep; 289(1-2):137-47. Epub 2006 May 23.
6. Low doses of vanadate and Trigonella synergistically regulate Na+/K + -ATPase activity and GLUT4 translocation in alloxan-diabetic rats. Mol Cell Biochem. 2006 Apr;285(1-2):17-27. Epub 2006 Apr 19.
7. Modulation of glucose transporter (GLUT4) by vanadate and Trigonella in alloxan-diabetic rats. Life Sci. 2006 Jan 18;78(8):820-4. Epub 2005 Nov 14.
8. Effect of supplementation of traditional medicinal plants on blood glucose in non-insulin-dependent diabetics: a pilot study. J Med Food. 2005 Winter;8(4):545-9.
9. Restoration of ultrastructural and biochemical changes in alloxan-induced diabetic rat sciatic nerve on treatment with Na3VO4 and Trigonella–a promising antidiabetic agent. Mol Cell Biochem. 2005 Oct; 278(1-2):21-31.
10. Supplementation of fenugreek leaves reduces oxidative stress in streptozotocin-induced diabetic rats. J Med Food. 2005 Fall;8(3):382-5.
11. Modulatory effect of fenugreek seed mucilage and spent turmeric on intestinal and renal disaccharidases in streptozotocin induced diabetic rats. Plant Foods Hum Nutr. 2005 Jun; 60(2):87-91.
12. The hypoglycaemic activity of fenugreek seed extract is mediated through the stimulation of an insulin signalling pathway. Br J Pharmacol. 2005 Sep; 146(1):41-8.
13. Trigonella foenum graecum seed powder protects against histopathological abnormalities in tissues of diabetic rats. Mol Cell Biochem. 2004 Nov; 266(1-2):151-9.
14. Genotoxicity testing of a fenugreek extract. Food Chem Toxicol. 2004 Nov; 42(11):1769-75.
15. Supplementation of fenugreek leaves lower lipid profile in streptozotocin-induced diabetic rats. J Med Food. 2004 Summer; 7(2):153-6.
16. Supplementation of fenugreek leaves to diabetic rats. Effect on carbohydrate metabolic enzymes in diabetic liver and kidney. Phytother Res. 2003 Dec; 17(10):1231-3.

Bitter Melon extracts possess anti-diabetic, hepato-renal protective and hypolipidemic effect in diabetic rats. Thus, Bitter Melon is alternative therapy that has primarily been used for lowering blood glucose levels in patients with diabetes mellitus. Beneficial effects were observed in Glycosaminoglycans (GAGs) metabolism during diabetes and it was postulated due to presence of dietary fibres present in bitter gourd and spent turmeric and presence of bioactive compounds in one or both of them (ref 4 ).

Experimental evidence was provided by research studies on dried bitter gourd powder in the diet at 10% level improved diabetic status signifying its beneficial effects during diabetes (ref 5). During diabetes structural and functional changes have been reported in alimentary tract and renal cortex which increases absorption of intestinal glucose and alternations in the activities of brush border dissacharidases. Feeding bitter gourd to diabetic rats showed positive influence on intestinal and renal dissacharidases making diabetic animals more tolerant to hyperglycermia (ref 6). Bitter Melon seeds extract- exerted rapid protective effects against lipid peroxidation by scavenging of free radicals thereby reducing the risk of diabetic complications (ref 7).

Memordica fruit extract and Sodium orthovandate exhibit hypolipedmic as well as hypoglycemic effect in diabetic rats (ref 8). According to research studies bitter melon has the potential to down-regulate insulin as well as preventative value with respect to a wide range of disorders. Parallels have been drawn between action of metformin and bitter melon including analogous effects on the hepatic activity certain enzymes of glucose-metabolism, increased expression of GLU4 in the plasma membrane of skeletal muscle and a tendency to prevent weight gain.

Aqueous extract powder of Bitter Melon, an edible vegetable, appears to be a safe alternative to reducing blood glucose. The aqueous extract powder of fresh unripe whole fruits was found to reduce fasting blood sugar by 48%, an effect comparable to that of Glibenclamide, a synthetic drug (ref 11).

The pharmacology, clinical efficiency, adverse effects, drug interactions of bitter melon have been studied in clinical trials (ref 12). Studies have been done to review the efficacy and safety of natural products commonly used for diabetes. Based on available evidence natural products like fenugreek, bitter melon, ginseng etc. can lower blood sugar in diabetic patients (ref 13).

Results of study on diabetic animals, suggests that changes in hepatic phase I and phase II
Drug metabolizing enzyme activities in STZ-induced diabetic animals may be associated with the altered expression of different CYP (Cytochrome 450) and GST (Glutathione-S-transferase) drug metabolizing isoenzymes.

It has been reported that ethyl acetate extract of bitter melon activated peroxisome proliferator receptors (PPRAs) alpha and gamma. PPRAs are ligand-dependent transcription factors that belong to the steroid hormone nuclear receptor family and control lipid and glucose homeostatis in the body (ref 2). Results of research study suggest that Bitter Melon juice and alcohol extracts caused a significant decrease in serum urea, creatinine, ALT, AST, AP, cholesterol and triglyceride levels (ref 3).

1. Momordica charantia (bitter melon) - Monograph. Altern Med Rev. 2007 Dec; 12(4):360-3.

2. Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARalpha in bitter gourd (Momordica charantia L.). J Biomed Sci. 2006 Nov; 13(6):763-72. Epub 2006 Sep 6.

3. Some toxicological studies of Momordica charantia L. on albino rats in normal and alloxan diabetic rats. J Ethnopharmacol. 2006 Nov 24; 108(2):236-42. Epub 2006 May 26.

4. Effect of bitter gourd and spent turmeric on constituents of glycosaminoglycans in different tissues in streptozotocin induced diabetic rats. Mol Cell Biochem. 2006 Jun; 286(1-2):53-8. Epub 2006 Mar 11.

5. Effect of bitter gourd (Momordica charantia) on glycaemic status in streptozotocin induced diabetic rats. Plant Foods Hum Nutr. 2005 Sep;60(3):109-12.

6. Bitter gourd (Momordica charantia) modulates activities of intestinal and renal disaccharidases in streptozotocin-induced diabetic rats. Mol Nutr Food Res. 2005 Aug; 49(8):791-6.

7. Antioxidant properties of Momordica Charantia (bitter gourd) seeds on Streptozotocin induced diabetic rats. Asia Pac J Clin Nutr. 2005; 14(2):153-8.

8. Combined treatment of sodium orthovanadate and Momordica charantia fruit extract prevents alterations in lipid profile and lipogenic enzymes in alloxan diabetic rats. Mol Cell Biochem. 2005 Jan; 268(1-2):111-20.

9. Does bitter melon contain an activator of AMP-activated kinase? Med Hypotheses. 2004; 63(2):340-3.

10. Evaluation of the efficacy of bitter gourd (Momordica charantia) as an oral hypoglycemic agent–a randomized controlled clinical trial. Indian J Physiol Pharmacol. 2003 Jul; 47(3):363-5.

11. Antihyperglycemic effects of three extracts from Momordica charantia. J Ethnopharmacol. 2003 Sep; 88(1):107-11.

12. Bitter melon (Momordica charantia): a review of efficacy and safety. Am J Health Syst Pharm. 2003 Feb 15; 60(4):356-9.

13. Natural products used for diabetes. J Am Pharm Assoc (Wash). 2002 Mar-Apr; 42(2):217-26.

14. Effect of bitter melon (Momordica charantia) fruit juice on the hepatic cytochrome P450-dependent monooxygenases and glutathione S-transferases in streptozotocin-induced diabetic rats. Biochem Pharmacol. 1996 Nov 22; 52(10):1639-42.