INTRODUCTION

Diabetes Mellitus (DM) can be found in almost every population in the world and epidemiological evidence suggests that, without effective prevention and control programmes, diabetes will likely continue to increase globally. Type 1 diabetes usually accounts for only a minority of the total burden of diabetes in a population but is increasing in incidence in both poor and rich countries. Type 2 diabetes constitutes about 85% to 95% of all diabetes in high-income countries and may account for an even higher percentage in low and middle-income countries. Type 2 diabetes is now a common and serious global health problem, which, for most countries, has evolved in association with rapid cultural and social changes, ageing populations, increasing urbanization, dietary changes, reduced physical activity and other unhealthy lifestyle and behavioral patterns (International Diabetes Federation, 2006).

Nowadays type 2 DM is one of the major public health concerns in both developing and developed countries in the Asian-Pacific region. It has become epidemic in a number of countries, particularly in newly industrialized nations. The direct and indirect social and economic costs of treating diabetes and its complications have the potential to cripple the countries’ healthcare budgets. In recent times, a new dimension has been added with the increasing appearance of type 2 diabetes in adolescents and even children (Asian-Pacific Type 2 Diabetes Policy Group, 2005).

Diabetes has recently been described as the perfect epidemic (Lau, 2001) is rapidly emerging as a global health care problem that threatens to reach pandemic levels by 2030. It is estimated that approximately 285 million people worldwide, or 6.6% adult have diabetes, 70% of whom live in low- and middle-income countries. This number is expected to increase by more than 50% in the next 20 years if preventive programmes are not put in place. By 2030, some 438 million people, or 7.8% of the adult population, are projected to have diabetes. The largest increases will take place in the regions dominated by developing economies (International Diabetes Federation, 2009).

Regardless of the type of diabetes, patients are required to control their blood glucose levels with medications and/or by adhering to an exercise program and a dietary plan. Insulin therapy by injection is given to those with type 1 DM and to some patients with type 2 DM. Patients with type 2 DM are usually placed on a restricted diet and are instructed to exercise, the purpose of which primarily is weight control. If diet and exercise fail to lower and stabilize blood glucose levels, oral anti-diabetic medication is prescribed. In some cases, insulin injections are necessary. Oral anti-diabetic agents exert their effects by various mechanisms: (1) stimulating beta cells in the pancreas to produce more insulin (sulfonylureas and meglitinides), (2) increasing the sensitivity of muscles and other tissues to insulin (thiazolidinediones), (3) decreasing gluconeogenesis by the liver (biguanides) and (4) delaying the absorption of carbohydrates from the gastrointestinal tract (alpha-glucosidase). These treatments are associated with adverse effects and some may produce toxic effects (e.g., thiazolidinediones may cause liver toxicity) (Dey et al., 2002).

Most of the oral therapeutic anti-diabetic agents are costly having with a lot of side effects. Moreover, it is very tough to the lower or middle income people to take costly anti-diabetic medication. As blood glucose monitoring is an essential task for patients suffering from diabetes; thus, beside diet and exercise any change caused by inexpensive herbal products to blood glucose levels without having any or fewer side effects may alter the amount of medication needed to control blood glucose.

CAUSES OF TYPE 2 DIABETES MELLITUS

There are a lot of causes (less insulin secretion by pancreas, insulin resistance etc.) and risk factors (age, obesity, ethnicity, strong family history of type 2 diabetes etc.) that are directly related to the pathogenesis of type 2 DM. Beside the risk factors the relation between lifestyle and diet habit with prevalence of type 2 DM has been proved by several articles (Asian-Pacific Type 2 Diabetes Policy Group, 2005).

In the past two decades, the rates of obesity have tripled in developing countries that have been adopting a Western lifestyle involving decreased physical activity and over consumption of cheap, energy-dense food (Hossain et al., 2007). The upsurge in obesity is closely linked to the increase in the prevalence of type 2 DM. About 90% of type 2 DM is attributable to excess weight (Hossain et al., 2007). Like developing countries over the last decade, profound changes in the quality, quantity and source of food consumed in many developed countries combined with a decrease in levels of physical activity have led to an increase in the prevalence of diabetes and its complications (Yach et al., 2006). Furthermore, some manifestations of Peripheral Diabetic Neuropathy (PDN) and cardiovascular disease in overweight and obese subjects develop at the stage of Impaired Glucose Tolerance (IGT) (Sumner et al., 2003; Reindel et al., 2004; Pittenger et al., 2005).

Several researches also showed the relation with the high fat diet, obesity and insulin resistance (Thounaojam et al., 2010). It is generally agreed that insulin resistance is an invariable accompaniment of obesity but that normoglycemia is maintained by compensatory hyperinsulinemia until the pancreatic β cells become unable to meet the increased demand for insulin, at which point type 2 DM begins. The mechanism by which β cells become unable to meet rising insulin demand has never been elucidated, primarily because of the unavailability of human pancreatic islets for appropriate study. However, post-mortem studies in patients with type 2 DM indicate that the β cell mass is reduced (Rahier et al., 1983). Some animal studies implicate fat deposition in islets as the cause of the β cell decompensation, so-called lipotoxicity (Lee et al., 1994). Excess fat in β cells and other nonadipocytes in this form of obesity is ascribed to the high plasma levels of Free Fatty Acids (FFAs) (Lee et al., 1994), coupled with a greatly enhanced capacity for lipogenesis (Lee et al., 1997). There is compelling in vitro evidence that the modest 5- to 10-fold increase in islet fat content that occurs in vivo in the prediabetic phase of the disease causes the compensatory β cell hyperplasia and hyperinsulinemia; a further increase in islet fat to ~50 times normal reverses the foregoing compensatory changes and causes β cell dysfunction, a reduction in the number of β cells and diabetes (Milburn et al., 1995; Hirose et al., 1996).

DIET AND LIFESTYLE TO PREVENT AND MANAGE TYPE 2 DIABETES MELLITUS

Type 2 diabetes mellitus is a common disease with substantial associated morbidity and mortality (Harris et al., 1998). Most adverse diabetes outcomes are a result of vascular complications, both at a macrovascular level (coronary artery disease, cerebrovascular disease, or peripheral vascular disease) and a microvascular level (retinopathy, nephropathy, or neuropathy) (UK Prospective Diabetes Study Group, 1998). Macrovascular complications are more common; up to 80% of patients with type 2 diabetes will develop or die of macrovascular disease (Wingard et al., 1993; Meigs et al., 1997) and the costs associated with macrovascular disease are an order of magnitude greater than those associated with microvascular disease (American Diabetes Association, 1998).

Because diabetes is defined by blood glucose levels, much of the attention in diabetes care focuses on the management of hyperglycemia. This has been magnified by the causal link between hyperglycemia and microvascular outcomes (Diabetes Control and Complications Trial Research Group, 1993). However, while some observational evidence suggests that level of glycemia is a risk factor for macrovascular disease (Laakso, 1996), experimental studies to date have not clearly shown a causal relationship between improved glycemic control and reductions in serious cardiovascular outcomes (Diabetes Control and Complications Trial Research Group, 1993). Given these results and the epidemiologic characteristics of diabetes complications, it would seem more logical to focus diabetes care on prevention of macrovascular complications rather than on glucose control and microvascular complications (Vijan and Hayward, 2003).

For this to prevent and maintain diabetes first we have to concentrate ourselves on diet and physical activities. Two landmark studies have confirmed that attainment of glycemic control as close to normal as possible is necessary for prevention of long term complications in both type 1 (Diabetes Control and Complications Trial Research Group, 1993) and type 2 (Ohkubo et al., 1995) diabetes and this requires an intensive approach to management. Nutrition is of utmost importance in intensive management and has often been described as the cornerstone of diabetes care (Kalergis et al., 2005). The main focus in the nutritional management of diabetes is to improve glycemic control by balancing food intake with endogenous and /or exogenous insulin levels. Historically, there have been several attempts to control the glycemic response to food, particularly carbohydrate-containing foods, including use of very low carbohydrate and starvation diets, artificial sweeteners and pharmacological preparations such as fast acting insulin and inhibitors of carbohydrate absorption (Kalergis et al., 2005). One way to classify the glycemic response of various carbohydrate-containing foods is Glycemic Index (GI). This term was first coined by Jenkins to describe the extent that blood glucose rises after a test food in comparison to a reference food, usually white bread (Jenkins et al., 1984).

Beside proper diet physical exercise is also necessary to maintain blood glucose level and to prevent type 2 diabetes related complications, such as nephropathy, retinopathy, arteriosclerotic heart disease and peripheral neuropathy, which most often result from the prolonged exposure to hyperglycemia (Kahn, 1995). Several animal studies have been showed the effect of physical exercise on maintenance of glucose level by improve glucose uptake through various mechanisms (Phillips et al., 1996; Ivy, 1997; Wojtaszweski et al., 1997; Heled et al., 2002).

MEDICINAL PLANTS TO PREVENT AND MANAGE TYPE 2 DIABETES MELLITUS

Oral anti-diabetic drugs are usually taken when diet and exercise failed to maintain hyperglycemia. Oral anti-diabetic agents are used to stimulate beta cells in the pancreas to produce more insulin (sulfonylureas and meglitinides), increase the sensitivity of muscles and other tissues to insulin (thiazolidinediones), decrease gluconeogenesis by the liver (biguanides), delay the absorption of carbohydrates from the gastrointestinal tract (alpha-glucosidase), treat hyperlipidemia and hyperinsulimea.

But presently, there is growing interest in herbal remedies due to the side effects associated with the oral hypoglycemic agents (therapeutic agent) for the treatment of diabetes mellitus (Day, 1998; Grover et al., 2002). In recent years, herbal medicines have started to gain importance as a source of hypoglycemic agents. Marles and Farnsworth (1995) estimated that more than 1000 plant species are being used as folk medicine for diabetes. Biological actions of the plant products used as alternative medicines to treat diabetes are related to their chemical composition. Herbal products or plant products are rich in phenolic compounds, flavonoids, terpenoids, coumarins and other constituents which show reduction in blood glucose levels (Jung et al., 2006; Hong-Fang et al., 2009). Several species of herbal drugs have been described in the scientific and popular literature as having antidiabetic activity (Valiathan, 1998). Several investigators reported anti-diabetic properties of various herbs not only in rats (Shanmugasundaram et al., 1990; Okabayashi et al., 1990) but also in humans (Hirata et al., 1992). Some of these showed the mechanisms by which medicinal plants produce anti-diabetic effects include: recovery of beta cells (Shanmugasundaram et al., 1990), inhibition of glucose absorption (Hirata et al., 1992), stimulation of insulin release (Sugihara et al., 2000) and increased glucose tolerance (Kar et al., 1999). Furthermore, the lipid lowering properties have been described (Shigematsu et al., 2001). Due to their perceived effectiveness, fewer side effects in clinical experience and relatively low costs, herbal drugs are now being prescribed widely by so many health practitioners (Verspohl, 2002). In the following paragraphs we describe the effect and mechanism of medicinal plants in maintenance of DM.

Ginseng (Panax ginseng): Several species are members of the Panax genus (Araliaceae family). These species include Panax quinquefolius (the American ginseng), Panax japonicus (the Japanese ginseng) and Panax ginseng (the Asian or Korean ginseng) (Ernst, 2002). Traditionally, the roots of the ginseng plant are used medicinally. Herbs in the Panax species contain ginsenosides that are unique to Panax. Ginsenosides are sapogenins (steroidal saponins) with a backbone chemical structure of either dammarane-type tetracyclic triterpene or oleananetype pentacyclic triterpene (Shibata, 2001). In addition to the ginsenosides, P ginseng contains at least 14 different glycans, known as panaxans (Konno et al., 1985; Oshima et al., 1985). Components in P ginseng alter blood glucose concentration by different mechanisms. Sever animal studies showed that the aqueous extract of ginseng root has the capability of producing hypoglycemia in both glucose-loaded healthy animals and in animals with experimentally induced diabetes, but not in healthy animals. This extract altered blood glucose levels by stimulating the biosynthesis of insulin by the pancreas and inducing the production of a glucose transporter in the liver (Waki et al., 1982; Ohnishi et al., 1996). The glycans in ginseng root also produce hypoglycemic effects in both normal animals and in those with experimentally induced diabetes (Ng and Yeung, 1985). The polysaccharides in ginseng lower blood glucose levels either by decreasing glucose production by the liver or by increasing the glucose use by tissues (Yang et al., 1990). Likewise, the polypeptides reduce blood glucose concentrations via their effect on adrenergic receptors (Wang et al., 1990).

Fenugreek (Trigonella foenum-graecum): The seeds of Trigonella foenum-graecum Linn. (Fabaceae) are traditionally used for their tonic, carminative, glucose-lowering functions and in the management of gastrointestinal ulcers (Zia et al., 2001). Several animal studies showed that the aqueous and alcoholic extracts of the seeds, as well as the seeds themselves, have a hypoglycemic effect when given orally (Raju et al., 2001; Puri et al., 2002; Yadav et al., 2008). Another animal study showed the hypoglycemic effect of the alcoholic extract of fenugreek in both healthy and diabetic rats, but the diabetic rats experienced a more pronounced decrease in blood glucose (Vats et al., 2002). Beside animal studies in a placebo-controlled clinical trial the hypoglycemic effect of hydro-alcoholic fenugreek seed extract has been proved in insulin resistant patients with type 2 DM (fasting glucose <200 mg dL^-1). In this trial one group received 1 g per day of hydro-alcoholic fenugreek seed extract for two consecutive months (12 patients) and another a placebo with dietary control and exercise (13 patients). All patients were insulin resistant. There was no statistical difference between the two groups with respect to fasting blood glucose levels or the two-hour post-glucose tolerance test at the end of the two-month treatment; however, a decrease in insulin secretion by the pancreas as well as improved sensitivity to insulin was observed after the fenugreek treatment but not with placebo (Gupta et al., 2001). In another study it has been showed that the patients with type 1 DM who received fenugreek seed powder in two divided doses (50 g each) with their lunch and dinner for 10 days experienced a significant reduction in their fasting blood glucose levels and a 54% reduction in 24 h urinary glucose secretion (Sharma et al., 1990). It appears that fenugreek can reduce blood glucose levels in patients with type 1 or type 2 DM, although its effect is less pronounced in patients with more severe diabetes. The effect of fenugreek on blood sugar in healthy individuals does not seem to be of importance. Clinicians counseling diabetic patients should be aware of this potential interaction between fenugreek and antidiabetic drugs (Al-Achi, 2005).

Bitter Melon (Momordica charantia): Momordica charantia Descourt. (Cucurbitaceae) is a complex plant medicine that has a remarkably long history of use, both as a food and as a medicine. In Asia and South America, this herb is widely used in folk medicine to treat diabetes. Several experimental animal studies support its effect on lowering blood glucose levels in both healthy and diabetic animals (Vikrant et al., 2001; Virdi et al., 2003). A clinical trial showed the effect of bitter melon juice that significantly improved glucose tolerance and the fried melon also improved glucose tolerance. Serum insulin levels did not increase, suggesting that bitter melon may have influenced hepatic or peripheral glucose disposal directly. This is doubly important because any agents that stimulate insulin release (so-called insulin secretagogues) may worsen insulin resistance in patients with NIDDM and accelerate beta-cell loss in patients with IDDM. Glycosylated hemoglobin also decreased in the patients suggesting an extrapancreatic action (Leatherdale et al., 1981).

In bitter melon there is a protein that is structurally and pharmacologically similar to bovine insulin (Baldwa et al., 1977). It is often referred to as v-insulin and research is ongoing to determine if this type of insulin may be suitable for patients who do not tolerate, or for philosophical reasons prefer not to use, animal sourced insulin. In a small study, 9 patients (6 with juvenile onset, 1 maturity onset and 2 asymptomatic IDDM) were given v-insulin subcutaneously. Five healthy and 5 patients with overt diabetes served as controls and were given a placebo injection. A hypoglycemic effect in the treatment group was observed that started 30-60 min after injection but peaked after 4-12 h (compared to 2-3 h for regular insulin) (Baldwa et al., 1977). In another study, subcutaneous v-protein produced a hypoglycemic effect in a small controlled study (n = 19) of juvenile and maturity onset IDDM. One juvenile patient who suffered side-effects when on bovine insulin (swelling, stomach pain and bouts of hypoglycemia) was maintained on v-protein for 5 months without experiencing any adverse effects (Khanna et al., 1981).

Gymnema (Gymnema sylvestre): G. sylvestre R. Br. (Asclepiadaceae) leaves contain triterpene saponins belonging to oleanane and dammarene classes. Oleanane saponins are gymnemic acids and gymnemasaponins, while dammarene saponins are gymnemasides. Besides this, other plant constituents are flavones, anthraquinones, hentri-acontane, pentatriacontane, α and β-chlorophylls, phytin, resins, dquercitol, tartaric acid, formic acid, butyric acid, lupeol, β-amyrin related glycosides and stigmasterol. The plant extract also tests positive for alkaloids. Leaves of this species yield acidic glycosides and anthroquinones and their derivatives (Dateo and Long, 1973).

Gymnemic acids have antidiabetic, antisweetener and anti-inflammatory activities. The antidiabetic array of molecules has been identified as a group of closely related gymnemic acids after it was successfully isolated and purified from the leaves of G. sylvestre (Liu et al., 1992). G. sylvestre leaves have been found to cause hypoglycemia in laboratory animals and have found a use in herbal medicine to help treat adult onset diabetes mellitus (NIDDM) (Shanmugasundaram et al., 1990; Okabayashi et al., 1990; Hirata et al., 1992).

The mechanisms by which G. sylvestre produce antidiabetic effects include: recovery of beta cells (Shanmugasundaram et al., 1990), inhibition of glucose absorption (Hirata et al., 1992; Shimizu et al., 1997), stimulation of insulin release (Sugihara et al., 2000) and increased glucose tolerance (Kar et al., 1999). Furthermore, the lipid lowering properties have been described (Wang et al., 1990; Shigematsu et al., 2001). However, it must be considered that all these studies were performed using a mixture of glycosides (Shimizu et al., 1997), a fraction denominated G. sylvestre (Shanmugasundaram et al., 1990; Okabayashi et al., 1990), alcoholic extract of leaves (Kar et al., 2003) and gymnemic acid (Hirata et al., 1992; Sugihara et al., 2000).

Banaba (Lagerstroemia speciosa): Lagerstroemia speciosa L. Pers. (Lythraceae), commonly known as banaba in the Philippines is a tropical flowering tree used as a folk medicine for the treatment of a myriad of diseases (De Padua et al., 1997). In the Philippines, the tea made from the leaves of L. speciosa has been used as a beverage for the treatment and prevention of diabetes mellitus (Quisumbing, 1978). Kakuda et al. (1996) studied banaba’s antidiabetic activity by preparing water and methanol extracts of the plant. After feeding the extracts to hereditary type 2 diabetic KK-Ay/Ta Jcl mice, they found that food containing either 5% of water extract (BE) or 3% of methanol extract was effective in reducing blood glucose and insulin levels (p<0.05) (Kakuda et al., 1996). In a second study it has been demonstrated that the extract possesses an anti-adipogenic activity by reducing weight gain on parametrial adipose tissue in female diabetic KKAY mice (Suzuki et al., 1999). Other in vitro studies using 3T3- L1 showed that the extract exhibits activities that stimulated both glucose transport and inhibited adipocyte differentiation (Liu et al., 2001; Bai et al., 2008). In rat adipocyte, leaves of L. speciosa increased the rate of glucose uptake and decreased the isoproterenol-induced glycerol release (Hayashi et al., 2002).

Tanquilut et al. (2009) showed the first physiological evidence that L. speciosa possesses anti-hyperglycemic effect in alloxan-induced diabetic mice that may offer a valuable therapeutic measure in the treatment of diabetes mellitus (Tanquilut et al., 2009). Moreover, clinical use of L. speciosa in diabetic patients has also been shown to suppress glucose level in a dose-dependent manner (Judy et al., 2003).

Holy basil (Ocimum sanctum): Ocimum sanctum Linn. (Labiatae) commonly known as Holy Basil. Different parts of this plant have been claimed to be valuable in a wide spectrum of diseases. Here the antidiabetic properties of O. sanctum are our main concern. The anti-diabetic properties of O. sanctum have been evaluated in several experimental animal models and very few studies on human are available. One animal study showed administration of fresh O. sanctum leaves (1 and 2 g day^-1) for four weeks exerted significant hypoglycaemic and uricosuric effects on fasting glucose and 24 h urine samples in experimental adult albino rabbits (Sarkar et al., 1990). Some other animal studies showed the hypoglycemic effect of different types of O. sanctum leaf extract in experimental rats with diabetes mellitus induced by alloxan (Giri et al., 1987) or by glucose and/or streptozotocin (Chattopadhyay, 1993; Chandra et al., 2008). O. sanctum also showed hypoglycaemic activity along with other herbal formulations. Dry O. sanctum leaf powder when fed at 1% of total diet for 30 days to the rats with diabetes induced by alloxan, fasting blood sugar, uronic acid, total amino acids, total cholesterol, triglyceride, phospholipids and total lipids reduced significantly (Rai et al., 1997a). Similarly, methanolic extract of O. sanctum when given to experimental animals at a dose of 200 mg kg^-1, bw for 30 days, the activities of glucokinase and hexokinase was increased significantly (Vats et al., 2004). It was also found that feeding of 200 mg kg^-1, body weight aqueous extract of whole O. sanctum plant for 60 days significantly delayed insulin resistance in fructose fed experimental mice (Reddy et al., 2008). The alcoholic extract and other organic solvent fraction’s extract has been found to stimulate insulin secretion from perfused rat pancreas, isolated islets and clonal pancreatic β-cells. The proposed mechanism of action for the secretion of insulin is that, O. sanctum extract is able to stimulate adenylate cyclase/ cAMP or the phosphatidylinositol or direct effect on exocytosis that induce mobilization of intracellular Ca⁺⁺ as well as promoting Ca⁺⁺ entry (Hannan et al., 2006).

In one of the initial randomized controlled clinical trails, anti-diabetic properties have been studied in 40 noninsulin dependent diabetes mellitus (NIDDM) patients. It was observed that taking dried O. sanctum leaf powder made from 2.5 g fresh leaves per day orally on empty stomach could reduce the fasting glucose level up to 21 mg dL^-1 and postprandial blood glucose by 15.8 mg dL^-1 (Agrawal et al., 1996). In another trial on 27 NIDDM patients, it was observed that supplementation of O. sanctum powder along with hypoglycaemic drugs for one month could significantly decrease the blood glucose, glycosylated proteins, total amino acids, uronic acid, triglycerides, Low Density Lipoprotein (LDL) and very Low Density Lipoprotein (VLDL), compared to control group on similar hypoglycaemic drugs. However, there was no significant change in High Density Lipoprotein (HDL) level (Rai et al., 1997b).

Periwinkle (Catharanthus roseus): Catharanthus roseus Linn. (Apocyanaceae) is known with various names (Madagascar periwinkle; Vinca rosea; Lochnera rosea) in all over the world. Water decoction of the leaves and/or the whole plant is used as household remedy for diabetes in several countries (Don, 1999). Several animal studies showed the antidiabetic activity of various types organic extracts of C. roseus (Swanston-Flatt et al., 1989; Chattopadhyay et al., 1991; Singh et al., 2001). As water decoction or fresh juice of leaves are used traditionally as antidiabetic, some animal studies also done with the juice of fresh leaves. In two animal studies researchers showed the hypoglycemic effect of the juice of fresh leaves of C. roseus in streptozotocin-induced (Ahmed et al., 2007) and alloxen induced (Nammi et al., 2003) diabetic animals. Moreover, the hypoglycemic effect of the powder of C. roseus leaves has also been proved clinically (Banakar et al., 2007).

Ivy Gourd (Coccinia indica): Coccina indica Wight and Am. has been used since ancient times as an antidiabetic drug by physicians who practice the Indian system of medicine known as Ayurveda. For this some researchers concentrate themselves to proof the antidiabetic effect of this plant. One animal study showed hypoglycemic effect of 95% ethanol extract of the leaves of C. indica. This effect was due in part to the inhibition of the key gluconeogenic enzyme glucose-6-phosphatase (Hossain et al., 1992). In another animal study showed that the oral administration of the isolated pectin from the fruit of the C. indica at a dose of 200 mg/100 g BW/day produced a reduction in glycaemia and an increase in liver glycogen. Glycogen synthetase activity was significantly increased. Incorporation of labeled glucose into hepatic glycogen was also found to be higher. A significant reduction in phosphorylase activity was noted in the pectin-administered groups (Kumar et al., 1993).

Garlic (Allium sativum L.) and Onion (Allium cepa L.): These two herbs are extensively used in many ethnic cuisines. Both garlic and onion belong to the genus Allium of the family Liliaceae. Garlic and onion have been shown to produce significant decreases in blood glucose concentrations in experimental animals. Healthy Wistar adult male rats showed significant decreases in blood glucose levels after they were fed a one-month diet containing 2% (wt/wt) garlic (Ahmed and Sharma, 1997). In healthy rabbits, the maximum glucose concentration following a subcutaneous glucose tolerance test was lower after oral treatment with garlic or onion (Roman-Ramos et al., 1995). Components in garlic and onion, S-allyl cysteine sulfoxide in garlic and S-Methyl Cysteine Sulfoxide (SMCS) in onion, were shown to cause the glucose-lowering effect seen in diabetic animals (Sheela et al., 1995; Kumari et al., 1995; Augusti and Sheela, 1996). SMCS was shown to improve the use of glucose as a result of an increase in insulin secretion by the pancreas (Kumari and Augusti, 2002).