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Essay on Bitter Gourd
Essay # 1. Origin of Bitter Gourd:
Bitter gourd is a vegetable indigenous to South America and Asia, used in native medicines of Asia and Africa, Oriental and Latin American countries. It is believed to be anti-dotal, anti-pyretic tonic, appetizing, stomachic, anti-bilious and laxative. It has been widely studied for its beneficial effects on blood glucose levels. Bitter gourd has been found to show anti-hyperglycemic activities when administered in experimental rats.
The hypoglycaemic efficacy in an aqueous extract of seeds of two varieties, namely a country and a hybrid variety of M. charantia clearly proved the anti-diabetic properties. Both the varieties showed safe and significant hypoglycaemic effects which were more pronounced in country variety compared to hybrid variety. The extract exerted rapid protective effects against lipid peroxidation by scavenging of free radicals thereby reducing the risk of diabetic complications. Metabolic and hypoglycaemic effects of bitter gourd extracts have been demonstrated in cell culture, animal, and human studies.
Active Components:
Bitter gourd contains bitter glycosides, saponins, alkaloids, reducing sugars, phenolic, oils, free acids, polypeptides, sterols, 17-amino acids including methionine and a crystalline product named p-insulin. It is reported to have hypoglycaemic activity in addition to being anti-haemorrhoidal, astringent, stomachic, emmenagogic, hepatic stimulant, anthelminthic and blood purifier.
Bitter gourd also contains charantin, vicine, and polypeptide-p, (anti-diabetic components) as well as other unspecific bioactive components such as anti-oxidants. Keller et al. (2011) discovered that a saponin-rich fraction isolated from M. cliarantia, stimulate insulin secretion in an in vitro, static incubation assay. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes the intracellular regeneration of active Cortisol from inert cortisone in key metabolic tissues, thus regulating ligand access to glucocorticoid receptors.
Out of the three anti-diabetic compounds namely, charantin, momordenol and momordicilin from bitter gourd, momordicilin was found to show minimum binding energy and thus found to be the most active compound in the respective target site.
Essay # 2. Effect of Bitter Gourd on Carbohydrate and Lipid Metabolism:
Bitter melon can suppress the visceral fat accumulation and inhibit adipocyte hypertrophy, which may be associated with marked down-regulated expressions of lipogenic genes in the adipose.
According to Chaturvedi (2012) the effects of bitter gourd including transport of glucose in the cells, transport of fatty acids in the mitochondria, modulation of insulin secretion, and elevation of levels of uncoupling proteins in adipose and skeletal muscles are similar to those of AMP-activated protein kinase (AMPK) and thyroxine. Therefore it is proposed that effects of bitter gourd on carbohydrate and fat metabolism are through thyroxine and AMPK.
There is strong evidence that increased adipose 11β-HSD1 activity may be an important a etiological factor in the current obesity and diabetes type 2 epidemics. Blum et al. (2012) showed that bitter gourd extract capsules contain at least one ingredient with selective 11 β-HSD1 inhibitory activity thus providing an interesting additional explanation for the well-documented anti-diabetic and hypoglycemic effects of bitter gourd.
The methanol extract of bitter gourd normalised blood glucose level, reduced triglyceride and LDL levels and increased HDL level in diabetic rats fed a high-fat and a low-carbohydrate diet. However, the animals reverted to a diabetic state once the extract was discontinued.
Bitter gourd consumption along with high fat diet ameliorates the negative influence of dietary fat on the body composition. Rats fed on the High fat + Bitter Melon (HF + BM) diet gained less weight and had less visceral fat than those fed the HF diet (P < 0.05). The addition of BM did not change apparent fat absorption. BM supplementation to the HF diet improved insulin resistance, lowered serum insulin and leptin but raised serum free fatty add concentration (P < 0.05). Chen et al. (2003) showed for the first time that BM reduces adiposity in rats fed a HF diet. BM appears to have multiple influences on glucose and lipid metabolism that strongly counteract the untoward effects of a high fat diet.
Shih et al (2009) demonstrated that bitter melon was effective in ameliorating the fructose diet-induced hyper-glycemia, hyper-leptinemia, hyper-insulinemia, and hyper-triglyceridemia as well as in decreasing the levels of free fatty acid. Bitter melon reversed fructose diet-induced hypo-adiponectinemia, which provides a therapeutic advantage to insulin resistance in improving insulin sensitivity. Additionally, bitter melon decreased the weights of epididymal and retroperitoneal white adipose tissue. Furthermore, they demonstrated that bitter melon significantly increased the mRNA expression and protein of glucose transporter 4 (GLUT4) in skeletal muscle.
Again, Roffey et al. (2007) reported that water-soluble component(s) in bitter gourd enhanced the glucose uptake at sub-optimal concentrations of insulin in 3T3-L1 adipocytes, which was accompanied by and might be the result of increased adiponectin secretion from the 3T3-L1 adipocytes. The mechanism of action of the extract in alloxan-induced diabetic rats seemed to be enhancing insulin secretion by the islets of Langerhans, reducing glycogenesis in liver tissue, enhancing peripheral glucose utilisation and increasing serum protein levels.
Further, the treatment restored the altered histological architecture of the islets of Langerhans. Hence, the biochemical, pharmacological and histo-pathological profiles of bitter gourd clearly indicate its potential anti-diabetic activity and other beneficial effects in amelioration of diabetes associated complications including hyper-lipidemia and obesity.
Essay # 3. Action of Bitter Gourd as an Anti-Diabetic Food:
Singh and Gupta (2007) observed the presence of small scattered islets among the acinar tissue when experimental diabetic animals were administered the acetone extract of bitter gourd fruit powder. These small scattered islets were suggestive of the neo formation of islets from pre-existing islet cells, which if proved by further studies will be beneficial for diabetic population.
Alleviation of pancreatic damage and an increase in the number of beta cells in neonatal diabetic rats fed with bitter gourd fruit extract was observed by Abdollahi et al. (2011). The islet size, total beta cell area and number of β-cells almost doubled in the diabetic rats treated with bitter gourd extract as compared to the untreated diabetic rats, and the extract-treated diabetic rat beta cells were found to be abundant with insulin granules.
Experiment conducted on rats and maturity onset diabetic patients, showed that bitter gourd improved glucose tolerance without any significant increase in serum insulin response, along with protective effect on development of diabetes induced cataract.
Singh et al. (2008) further observed that the blood glucose once lowered by the treatment with bitter gourd fruit extract remained static even after discontinuation of the extract for 15 days and the blood sugar never fell below normal values even with a high dose of this extract. Kumar et al. (2009) demonstrated the significance of Glut- 4, PPAR gamma and PI3K up-regulation by bitter gourd in augmenting the glucose uptake and homeostasis.
According to Sitasawad et al. (2000) feeding the aqueous juice of bitter gourd fruit resulted in reduction of STZ-induced hyperglycemia in mice. It also markedly reduced the STZ-induced lipid peroxidation in pancreas of mice, RIN cells and islets. Further, it reduced the STZ-induced apoptosis in RIN cells indicating the mode of protection of bitter gourd juice on RIN cells, islets and pancreatic beta-cells.
Mode of Ingestion:
Sitasawad et al. (2000) confirmed hypoglycemic effect of BF juice and provides sufficient documentation to define its role and action for its potential and promising use in treating diabetes. In non-insulin dependent diabetic patients (Ahmad et al, 1999) the juice of bitter gourd produced significant reduction in fasting as well as post prandial blood sugars after an oral glucose tolerance test.
Cummings et al. (2004) found the fruit juice to act like insulin to exert its hypoglycaemic effect and stimulate amino acid uptake into skeletal muscle cells just like insulin. Significant improvement in fasting blood glucose, serum insulin, β-cell number and function was observed with administration of bitter gourd extract to the diabetic rat model.
In a human study, Baldwa and his team, as early as 1977, administered insulin like compound obtained from the bitter gourd fruit and tissue culture. This compound was homologous to animal insulin and showed consistent hypoglycaemic effect on diabetic subjects.
It showed the onset of action within 30-60 min and the peak effect of six hours after the administration of the dose without any hyper-sensitivity reaction among the subjects. Time course experiments performed in rat adipocytes by Yibchokanun (2006) revealed that M. charantia protein extract significantly increased glucose uptake after 4 and 6 h of incubation. Thus, the M. charantia protein extract, a slow acting chemical, exerted both insulin secretagogue and insulin mimetic activities to lower blood glucose concentrations in vivo.
Extracts of fruit pulp, seed, leaves and whole plant was shown to have hypoglycaemic effect in various animal models. Polypeptide p, isolated from fruit, seeds and tissues of bitter gourd showed significant hypoglycaemic effect when administered subcutaneously to langurs and humans. 200 mg/ kg ethanolic extract showed an anti-hyperglycemic effect in normal and STZ diabetic rats. This may be because of inhibition of glucose-6-phosphatase besides fructose-1, 6-biphosphatase in the liver and stimulation of hepatic glucose-6-phosphate dehydrogenase activities.
Dried bitter gourd powder at 10 per cent level in the diet in streptozotocin induced diabetic rats brought down the fasting blood glucose level by about 30 per cent. In addition, bitter gourd supplementation alleviated the rise in water consumption, urine volume and urine sugar during diabetes by about 30 per cent as compared to the controls. Renal hyper-trophy was higher in diabetic controls and bitter gourd supplementation partially, but effectively prevented it by 38 per cent. Increased glomerular filtration rate in diabetes was significantly reduced by 27 per cent in the experimental group.
Transdermal patches made up of bitter gourd extract showed improvement in blood glucose parameters of experimental rats without any incidence of skin irritation or reaction.
Synergistic Effect:
A combination of extracts of bitter gourd and fenugreek when administered to alloxan induced diabetes rats for 30 days showed improvement in the fasting blood sugars along with protection of the heart, kidneys and liver tissue against oxidative stress.
β-Glucan purified from oats (OG) and bitter melon (MC), water extracts have shown favorable effects on diabetes and its complications. In variable compositions (OG:MC = 1:1, 1:2, 1:4, 1:6, 1:8, 1:10, 2:1, 4:1, 6:1, 8:1, 10:1) the extracts were administered orally once a day for 28 days following 7 days post streptozotocin (STZ) dosing. The changes of hyperglycaemia, diabetic nephropathy, hepatopathy, and hyper-lipemia observed as the result of STZ-induced diabetes were dramatically decreased in the OG and MC single-dosing group, and all composition groups. Among variable compositions, the OG: MC 1:2 mixed group showed the most synergic effects.
The ethanol extract of E. jambolana seeds, water extract of M. charantia fruits, ethanol extract of G. sylvestre leaves, and water extract of fenugreek seeds have higher hypoglycaemic and anti-hyperglyceamic potential and may be used as complementary medicine to treat the diabetic population by significantly reducing the dosage of standard drug.
Essay # 4. Comparison of Bitter Gourd with Hypoglycaemic Drugs:
Diabetes mellitus is associated with an increase in sialic acid concentration along with other complications. Comparison of serum sialic acid concentration of patients, following bitter melon and rosiglitazone treatment revealed no significant difference but it was shown that bitter melon could be more effective in the management of diabetes and its related complications as compared to rosiglitazone.
The seed varieties of bitter gourd were more effective than the glibenclamide, a known synthetic drug in normalizing the impaired oxidative stress in streptozotocin induced-diabetic rats.
Bitter melon fruit aqueous extract reduced the blood glucose level similar to glibenclamide and increased the serum insulin level in the treated diabetic rats. The fruit extract alleviated pancreatic damage and increased the number of β-cells in the diabetic treated rats suggesting that oral feeding of the fruit extract may have a significant role in the renewal of pancreatic β-cells in the diabetic control group rats.
Bitter melon may have additive effects when taken with other glucose-lowering agents. Yadav et al (2005) found that the fruit extract and sodium orthovanadate, a well-known insulin mimetic and an anti-diabetic compound exhibited hypo-lipidemic as well as hypoglycemic effect in diabetic rats and their effect was pronounced when administered in combination.
Bitter melon significantly reduced fructosamine levels from baseline among patients with type 2 diabetes who received 2,000 mg/day. However, the hypoglycemic effect of bitter melon was less than metformin (1,000 mg/day). Huang et al. (2008) showed that Bitter melon can reduce insulin resistance as effective as the anti-diabetic drug thiazolidinedione.
In spite of the fact that numerous pre-clinical studies have documented the anti-diabetic and hypo-glycaemic effects of bitter gourd through various postulated mechanisms, Leung et al. (2009) called for better-designed clinical trials to further elucidate its possible therapeutic effects.
Safety:
Bitter gourd has the potential to become a component of the diet or a dietary supplement for diabetic and pre-diabetic patients. According to Virdi et al. (2003) the aqueous extract powder of fresh unripe whole fruits did not show any signs of nephrotoxicity and hepato-toxicity as judged by histological and biochemical parameters. Thus the aqueous extract powder of M. charantia appears to be a safe alternative to reduce blood glucose.
Malik et al. (2011) also reported that bitter gourd has potent neuro-protective activity against global cerebral ischemia-reperfusion induced neuronal injury and consequent neurological deficits in diabetic mice. Snee et al. (2011) suggested that incorporating variety of foods along with bitter gourd in commonly consumed recipes can mask bitter taste of bitter melon. Furthermore, providing positive health information can elicit a change in the intent to consume bitter melon-containing dishes despite mixed palatability results.