Effect of Eugenia Jambolana seed kernel on antioxidant defense system in streptozotocin-induced diabetes in rats

Increased oxidative stress has been suggested to be involved in the pathogenesis and progression of diabetic tissue damage. The aim of this study was to investigate the effect of ethanolic extract of Eugenia jambolana seed kernel on antioxidant defense systems of plasma and pancreas in streptozotocin-induced diabetes in rats. The levels of glucose, vitamin-C, vitamin-E, ceruloplasmin, reduced glutathione and lipidperoxides were estimated in plasma of control and experimental groups of rats. The levels of lipidperoxides, reduced glutathione and activities of superoxide dismutase, catalase and glutathione peroxidase were assayed in pancreatic tissue of control and experimental groups of rats. A significant increase in the levels of plasma glucose, vitamin-E, ceruloplasmin, lipid peroxides and a concomitant decrease in the levels of vitamin-C, reduced glutathione were observed in diabetic rats. The activities of pancreatic antioxidant enzymes were altered in diabetic rats. These alterations were reverted back to near normal level after the treatment with Eugenia jambolana seed kernel and glibenclamide. Histopathological studies also revealed that the protective effect of Eugenia jambolana seed kernel on pancreatic beta-cells. The present study shows that Eugenia jambolana seed kernel decreased oxidative stress in diabetic rats, which inturn may be due to its hypoglycemic property.     

A krill oil supplemented diet suppresses hepatic steatosis in high-fat fed rats

Krill oil (KO) is a dietary source of n-3 polyunsaturated fatty acids, mainly represented by eicosapentaenoic acid and docosahexaenoic acid bound to phospholipids. The supplementation of a high-fat diet with 2.5% KO efficiently prevented triglyceride and cholesterol accumulation in liver of treated rats. This effect was accompanied by a parallel reduction of the plasma levels of triglycerides and glucose and by the prevention of a plasma insulin increase. The investigation of the molecular mechanisms of KO action in high-fat fed animals revealed a strong decrease in the activities of the mitochondrial citrate carrier and of the cytosolic acetyl-CoA carboxylase and fatty acid synthetase, which are both involved in hepatic de novo lipogenesis. In these animals a significant increase in the activity of carnitine palmitoyl-transferase I and in the levels of carnitine was also observed, suggesting a concomitant stimulation of hepatic fatty acid oxidation. The KO supplemented animals also retained an efficient mitochondrial oxidative phosphorylation, most probably as a consequence of a KO-induced arrest of the uncoupling effects of a high-fat diet. Lastly, the KO supplementation prevented an increase in body weight, as well as oxidative damage of lipids and proteins, which is often found in high-fat fed animals.     

壬基酚对鲫鱼原代肝细胞增殖和抗氧化功能的影响

研究了不同浓度壬基酚对鲫鱼肝细胞增殖和抗氧化系统的影响.结果表明：各试验浓度壬基酚均能抑制鲫鱼肝细胞的增殖,其中高浓度的壬基酚（10^-3 mol·L^-1）对细胞增殖的抑制作用极其显著,肝细胞形态发生明显改变;壬基酚破坏了鲫鱼肝细胞抗氧化系统的平衡,经壬基酚处理后的肝细胞超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性均受到抑制,而羟自由基的含量升高;壬基酚对原代鲫鱼肝细胞造成氧化损伤,引起培养液中丙二醛（MDA）含量升高.壬基酚诱导的氧化胁迫对原代鲫鱼肝细胞产生了一系列的体外毒性效应.     

Oral administration of levan polysaccharide reduces the alloxan-induced oxidative stress in rats

This study aimed to evaluate the effect of a polysaccharide named levan, which was produced by new isolated bacteria, on oxidative stress and hyperglycemia in alloxan-induced diabetic rats. Levan polysaccharide was given in drinking water for 60 days at a daily dose equivalent to 2%. The oral administration of levan in diabetic rats caused a decrease in glucose level in plasma and an increase of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities in both pancreas and liver. Furthermore, a protective action against hepatic and pancreatic toxicity in diabetic rats was clearly observed. Furthermore, a significant decrease in hepatic and pancreatic indices toxicity was observed, i.e., alkalines phosphatases (ALP), aspartate and lactate transaminases (AST and ALT), lactate deshydrogenases (LDH) activities and the thiobarbituric acid-reactive substances (TBARs). These beneficial effects of levan were confirmed by histological findings in hepatic and pancreatic tissues of diabetic rats. This study demonstrates for the first time that levan is efficient in inhibiting hyperglycemia and oxidative stress induced by diabetes and suggests that administration of levan may be helpful in the prevention of diabetic complications associated with oxidative stress.     

Low-carbohydrate diet and oxidative stress in diabetic and nondiabetic rats

Hyperglycemia of diabetes has been implicated in increased tissue oxidative stress, with consequent development of secondary complications. Thus, stabilizing glucose levels near normal levels is of utmost importance. Because diet influences glycemic control, this study investigated whether a low-carbohydrate (5.5%) diet confers beneficial effects on the oxidative status of the heart, kidney, and liver in diabetes. Male and female normal and diabetic rats were fed standard chow (63% carbohydrates) or low-carbohydrate diet for 30 days. Elevated glucose, HbA(1c), and alanine and aspartate aminotransferases in diabetic animals were reduced or normalized by the low-carbohydrate diet. While diabetes increased cardiac activities of glutathione peroxidase and catalase, low-carbohydrate diet normalized cardiac glutathione peroxidase activity in diabetic animals, and reduced catalase activity in females. Diabetic rats fed low-carbohydrate diet had altered activities of renal glutathione reductase and superoxide dismutase, but increased renal glutathione peroxidase activity in diabetic animals was not corrected by the test diet. In the liver, diabetes was associated with a decrease in catalase activity and glutathione levels and an increase in glutathione peroxidase and gamma-glutamyltranspeptidase activities. Decreased hepatic glutathione peroxidase activity and lipid peroxidation were noted in diet-treated diabetic rats. Overall, the low-carbohydrate diet helped stabilize hyperglycemia and did not produce overtly negative effects in tissues of normal or diabetic rats.     

Effects of antilipolytic agents on rat liver peroxisomes and peroxisomal oxidative activities

The mechanisms involved in the inhibitory effects of antilipolytic agents on rat liver peroxisomal fatty acid oxidative activity have been explored. Treatment of fasting rats with antilipolytic drugs (either 3,5-dimethylpyrazole (12 mg/kg body weight) or Acipimox (25 mg/kg body weight)) resulted in a decrease in free fatty acid and glucose plasma levels within 5–10 and in a significant increase in the plasma glucagon to insulin ratio within 15. Changes in the fatty acid oxidative activity appeared with a 2.5–3 h delay and were then very rapid (a 30–40% decrease in the activity occured in additional 2 h). Many peroxisomal enzyme activities (including non-β-oxidative activities such as uricase and D-amino acid oxidase) exhibited similar changes with the same delay. Simultaneously with the enzyme changes, at the electron microscope level many autophagic vacuoles were detected in the liver cells, often containing peroxisomal structures. Glutamine, an inhibitor of proteolysis in vivo, prevented the decrease in enzyme activities. It was concluded that the decrease in peroxisomal enzyme activities may be the consequence of enhanced peroxisome degradation due to the stimulation of autophagic processes in liver cells.     

Comparative and combined effect of chlorogenic acid and tetrahydrocurcumin on antioxidant disparities in chemical induced experimental diabetes

The present study evaluates the combined effect of tetrahydrocurcumin and chlorogenic acid on oxidative stress in streptozotocin–nicotinamide-induced diabetic rats. Rats were rendered diabetic by a single intraperitoneal injection (i.p) of streptozotocin (45 mg/kg BW), 15 min after an i.p injection of nicotinamide (110 mg/kg BW). The levels of fasting plasma glucose and insulin were estimated. As an index of oxidative stress, the levels of enzymic antioxidants and lipid peroxidation products were analyzed in liver and kidney. Diabetic rats showed an increase in the levels of fasting plasma glucose, lipid peroxidative products such as thiobarbituric acid reactive substances and lipid hydroperoxides and a decrease in plasma insulin, and enzymic antioxidants viz., superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase. Combined administration of tetrahydrocurcumin (80 mg/kg BW) and chlorogenic acid (5 mg/kg BW) to diabetic rats for 45 days, reversed the biochemical changes to near normal. The above findings were supported by histological observations of the liver and kidney. Together the present study clearly reflects that combined dosage of tetrahydrocurcumin and chlorogenic acid augments enzymic antioxidants with a concomitant decrease in lipid peroxidation and protects against streptozotocin–nicotinamide-induced type 2 diabetes in experimental rats.     

Reduction of diabetes-induced oxidative stress by phosphodiesterase inhibitors in rats

Increased oxidative stress has been suggested to be involved in the pathogenesis and progression of diabetic tissue damage. The aim of this study was to investigate the effect of different phosphodiesterase inhibitors on lipid peroxidation and total antioxidant capacity (TAC) of plasma in streptozotocin-induced diabetic rats (Rattus norvegicus). Rats became diabetic by a single administration of streptozotocin (STZ, 45 mg/kg). The effects of 15-days treatment by milrinone, sildenafil, and theophylline as cyclic-AMP and -GMP phosphodiesterase inhibitors (PDEIs) on diabetes-induced oxidative stress were studied. The levels of glucose, malonedialdehyde (MDA) the by product of lipid peroxides, and TAC (FRAP test) were estimated in plasma of control and experimental groups of rats. A significant increase in the levels of plasma glucose, and MDA and a concomitant decrease in the levels of TAC were observed in diabetic rats. These alterations were reverted back to near normal level after the treatment with PDEIs. Treatment of diabetic rats by PDEIs reduced MDA levels and increased TAC in the order of milrinone>sildenafil>theophylline. In conclusion, the present investigation show that PDIS possesses antioxidant activities, which may be attributed to their enhancing effect on cellular cyclic nucleotides contributing to the protection against oxidative stress in streptozotocin-induced diabetes. Exact mechanism of protective actions of cAMP- and cGMP-phosphodiesterase remains to be elucidated by further studies. This finding may suggest a place for PDEIs in maintaining health in diabetes.     

Antidiabetic activity of levan polysaccharide in alloxan-induced diabetic rats

This study aims to examine the effects of polysaccharide levan on oxidative stress and hyperglycemia in alloxan-induced diabetic rats. Levan, used in this study, was a microbial levan synthetisized by a non pathogenic bacteria recently isolated and identified as Bacillus licheniformis. Animals were allocated into four groups of six rats each: a control group (Control), diabetic group (Diab.), normal rats received levan (L) and diabetic rats fed with levan (DL). Treated diabetic rats were administrated with levan in drinking water through oral gavage for 60 days. The administration of polysaccharide levan in diabetic rats caused a significant increase in glycogen level by 52% and a decrease in glucose level in plasma by 52%. Similarly, the administration of polysaccharide levan in diabetic rats caused a decrease in the thiobarbituric acid-reactive substances (TBARS) by 31%, 41%, 39% and 25%, an increase in superoxide dismutase (SOD) by 40%, 50%, 44% and 34%, and in catalase (CAT) by 18%, 20%, 12% and 18% in liver, kidney, pancreas and heart, respectively. Furthermore, a significant decrease in hepatic and renal indices toxicity was observed, i.e. alkalines phosphatases (ALP), aspartate and lactate transaminases (AST and ALT) activities, total bilirubin, creatinine and urea levels by 19%, 31%, 32%, 36%, 37% and 23%, respectively. The results show that administration of polysaccharide levan can restore abnormal oxidative indice near normal levels. This study demonstrates, for the first time, that polysaccharide levan is efficient in inhibiting hyperglycemia and oxidative stress induced by diabetes and suggests that levan supplemented to diet may be helpful in preventing diabetic complications in adult rats.     

Rutin improves glucose homeostasis in streptozotocin diabetic tissues by altering glycolytic and gluconeogenic enzymes

The role of rutin on carbohydrate metabolism in normal and streptozotocin (STZ)-induced diabetic rats was investigated in the present study. Administration of STZ led to a significant (p <0.05) increase in fasting plasma glucose and a decrease in insulin levels. The content of glycogen significantly (p <0.05) decreased in liver and muscle, but increased in kidney. The activity of hexokinase decreased whereas the activities of glucose-6-phosphatase and fructose-1,6-bisphosphatase significantly (p <0.05) increased in the tissues. Oral administration of rutin (100 mg/kg) to diabetic rats for a period of 45 days resulted in significant (p <0.05) alterations in the parameters studied but not in normal rats. A decrease of plasma glucose and increase in insulin levels were observed along with the restoration of glycogen content and the activities of carbohydrate metabolic enzymes in rutin-treated diabetic rats. The histopathological study of the pancreas revealed the protective role of rutin. There was an expansion of the islets and decreased fatty infiltrate of the islets in rutin-treated diabetic rats. In normal rats treated with rutin, we could not observe any significant change in all the parameters studied. Combined, these results show that rutin plays a positive role in carbohydrate metabolism and antioxidant status in diabetic rats.     

Effect of nonylphenol on growth of Neurospora crassa and Candida albicans.

The effects of the nonionic surfactant nonylphenol on the growth and morphologies of the filamentous fungus Neurospora crassa and the diploid yeast Candida albicans have been examined. Nonylphenol inhibited respiration and growth of N. crassa, effecting a 10-fold decrease in organism yield at 25 microM. Severe morphological defects were also induced: cell shape was abnormal and apical dominance was lost. Nonylphenol monoethoxylate (the parent compound of nonylphenol) was a less potent growth inhibitor and morphogen. The growth of the yeast form of C. albicans was sensitive to nonylphenol (inducing an order of magnitude decrease in specific growth rate with a 10-fold increase in dose concentration) but not nonylphenol monoethoxylate. Similarly, C. albicans ATP content was reduced and glucose-induced extracellular acidification was inhibited only by nonylphenol. Although estrogens may induce the dimorphic transition of C. albicans, nonylphenol (as an environmental estrogen mimic) failed to trigger germ tube formation under nonpermissive conditions and inhibited it under permissive conditions. The effects of nonylphenol are most readily explained as the result of uncoupling of respiration, which produces multiple physiological effects.     

The effect of stress or glucose feeding on hepatic tyrosine aminotransferase activity and liver and plasma tyrosine level of intact and adrenalectomized rats.

The increase of hepatic tyrosine aminotransferase and the fall of plasma tyrosine in rats subjected to immobilization is reconfirmed. Moreover, the same effects three hrs after exposuing the animals to 400 revolutions in Noble-Collip drums are described. However, in bilaterally adrenalectomized rats both hepatic tyrosine aminotransferase and plasma tyrosine remain unchanged after injury and the liver tyrosine level increase. Finally, in animals fed overnight exclusively with 15% glucose solution the well-known decrease of hepatic tyrosine aminotransferase was found paralleled by increased plasma tyrosine levels. A regulatory role of tyrosine aminotransferase in establishing the level of tyrosine in plasma is suggested.     

Effect of galangin supplementation on oxidative damage and inflammatory changes in fructose-fed rat liver

The study examined the effects of galangin (GA) on oxidative stress, inflammatory cytokine levels and nuclear factor-kappa B (NF-κB) activation in fructose-fed rat liver. Adult male albino Wistar rats were divided into 4 groups. Groups 1 and 4 received the control diet containing starch as the source of carbohydrate while groups 2 and 3 were fed a diet containing fructose. Groups 3 and 4 additionally received GA (100 μg/kg, p.o) from the 15th day. At the end of 60 days, the levels of plasma glucose, insulin and triglycerides, insulin sensitivity indices and oxidative stress markers in the liver were determined. Cytokines of interest were assayed by ELISA and RT-PCR and NF-κB p65 nuclear translocation by Western blot and RT-PCR. Compared to control diet-fed animals, fructose-fed animals developed hyperglycemia, hyperinsulinemia, hypertriglyceridemia and insulin resistance (IR) (all p < 0.01). GA prevented the rise in plasma glucose, insulin and triglycerides and improved insulin sensitivity. Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in plasma and the mRNA and protein levels of TNF-α and transforming growth factor-β1(TGF-β₁) in liver were significantly higher in fructose-fed rats than control rats. However, treatment with GA downregulated the expression of these cytokines. Translocation of NF-κB into the nucleus was also increased in fructose diet-fed animals, which was prevented by GA. These results suggest that GA prevents oxidative damage and has a downregulatory effect on the inflammatory pathway in liver of fructose-fed rats.     

Effects of high sucrose diet on insulin-like effects of vanadate in diabetic rats

The insulin-like effects of vanadate were compared in streptozotocin-induced diabetic rats fed on high starch control and high sucrose diets for a period of six weeks. Diabetic rats in both diet groups were characterized by hypoinsulinemia, hyperglycemia (6.8–7.0 fold increase) and significant decreases (p<0.001) in the activities of glycogen synthase, phosphorylase and lipogenic enzymes, ATP-citrate lyase, glucose 6-phosphate dehydrogenase and malic enzyme in liver. There were no diet-dependent differences in these abnormalities. However, the insulin-mimetic agent vanadate was more effective in diabetic rats fed sucrose diet as compared to animals fed control starch diet. Vanadate administration resulted in 30% and 64% decreases in plasma glucose levels in diabetic rats fed control and sucrose diets, respectively. The activities of glycogen synthase (active) and phosphorylase (active and total) were restored significantly by vanadate in control (p<0.05–0.01) and sucrose (p<0.001) diets fed diabetic rats. This insulin-mimetic agent increased the activities of hepatic lipogenic enzymes in control diet fed rats to 38–47% of normal levels whereas in sucrose fed group it completely restored the activities. Sucrose diet caused a distinct effect on the plasma levels of triacylglycerol (4-fold increase) and apolipoprotein B (2.8-fold increase) in diabetic rats and vanadate supplementation decreased their levels by 65–75%. These data indicate that vanadate exerts insulin-like effects in diabetic rats more effectively in sucrose fed group than the animals fed control diet. In addition, vanadate also prevents sucrose-induced hypertriglyceridemia.     

Quercitrin a bioflavonoid improves the antioxidant status in streptozotocin: induced diabetic rat tissues

Quercitrin, a bio flavonoid, was investigated for its antioxidant potential in streptozotocin (STZ)-induced diabetic rats. Rats were induced diabetic by a single intraperitoneal injection of streptozotocin (50 mg/kg). The levels of fasting plasma glucose and insulin were estimated. Lipid peroxidative products and antioxidants were estimated in pancreas, liver, and kidney. Histopathological studies were carried out in these tissues. A significant (P < 0.05) increase in the levels of fasting plasma glucose and lipid peroxidative products (thiobarbituric acid reactive substances and lipid hydroperoxides) and a significant (P < 0.05) decrease in plasma insulin, enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase), and nonenzymic antioxidants (reduced glutathione, vitamin C, and E) in diabetic pancreas, liver, and kidney were observed. Oral administration of quercitrin (30 mg/kg) for a period of 30 days significantly (P < 0.05) decreased fasting plasma glucose, increased insulin levels, and improved the antioxidant status of diabetic rats by decreasing lipid peroxidative products and increasing enzymic and nonenzymic antioxidants. Normal rats treated with quercitrin (30 mg/kg) showed no significant (P < 0.05) effect on any of the parameters studied. Histopathological studies of the pancreas, liver, and kidney showed the protective role of quercitrin. Thus, our study clearly shows that quercitrin has antioxidant effect in STZ-induced experimental diabetes.     

Effects of hypo and hyperthyroidism on the response to glucose loading of blood glucose, ketones and insulin and liver glycogen as studied in the fasted rat

After receiving an i.p. glucose load, 24 h fasted thyroidectomized rats showed a progressive increase in blood glucose and a slow decrease in blood ketone bodies. Both liver glycogen and plasma insulin levels showed no differences within 60 min of the glucose administration. It is suggested that the glucose intolerance in these animals is partly due to an insulin deficiency. Thyroidectomized rats treated daily with 25 microgram of L-thyroxine/100 g body weight for 40 days responded to the glucose test with a supranormal and more persistent elevation of blood glucose but with a faster and a greater fall in blood ketone bodies, as compared to controls. Sixty min after the glucose loading, liver glucogen levels were lower and plasma insulin were slightly higher than controls. It is suggested that a diminished extraction of glucose during transhepatic passage can be responsible for the impaired glucose tolerance observed in the hyperthyroid animals.     

The effects of a load of phen?lalanine on glucose metabolism

The clinical and experimental hyperphenylalaninemic conditions seem associated with disorders of carbohydrates metabolism. Examples are the increased liver glucose turnover and the glycogen depletion under Phenylalanine load and the hyperexcretion of glucose in the urine of PKU children. We studied the effects of an acute load of Phenylalanine on Glucose-3-H3 kinetics and plasma glucose levels in adult male Wistar rats. The effects of the load were very slow and after 40 minutes we observed an increase in the rate of plasma glucose production (Ra), that in normal animals in an almost exclusive liver function. As result of this glucose production there was a modest increase in plasma glucose levels.     

Experimental hyperprolinemia induces mild oxidative stress, metabolic changes, and tissue adaptation in rat liver

The present study investigated the effects of chronic hyperprolinemia on oxidative and metabolic status in liver and serum of rats. Wistar rats received daily subcutaneous injections of proline from their 6th to 28th day of life. Twelve hours after the last injection the rats were sacrificed and liver and serum were collected. Results showed that hyperprolinemia induced a significant reduction in total antioxidant potential and thiobarbituric acid-reactive substances. The activities of the antioxidant enzymes catalase and superoxide dismutase were significantly increased after chronic proline administration, while glutathione (GSH) peroxidase activity, dichlorofluorescin oxidation, GSH, sulfhydryl, and carbonyl content remained unaltered. Histological analyses of the liver revealed that proline treatment induced changes of the hepatic microarchitecture and increased the number of inflammatory cells and the glycogen content. Biochemical determination also demonstrated an increase in glycogen concentration, as well as a higher synthesis of glycogen in liver of hyperprolinemic rats. Regarding to hepatic metabolism, it was observed an increase on glucose oxidation and a decrease on lipid synthesis from glucose. However, hepatic lipid content and serum glucose levels were not changed. Proline administration did not alter the aminotransferases activities and serum markers of hepatic injury. Our findings suggest that hyperprolinemia alters the liver homeostasis possibly by induction of a mild degree of oxidative stress and metabolic changes. The hepatic alterations caused by proline probably do not implicate in substantial hepatic tissue damage, but rather demonstrate a process of adaptation of this tissue to oxidative stress. However, the biological significance of these findings requires additional investigation.     

Protective effect of ascorbic acid against lipid peroxidation and oxidative damage in cardiac microsomes

Effects of feeding sucrose rich diet supplemented with and without the insulinmimetic agent vanadate for a period of six weeks were studied in rats. Sucrose diet caused hypertriglyceridemia (140% increase), hyperinsulinemia (120% increase) and significant elevations in the levels of glucose (p<0.001) and cholesterol (p<0.05) in plasma as compared to control starch fed rats. Activities of hepatic lipogenic enzymes, ATP-citrate lyase, glucose 6-phosphate dehydrogenase and malic enzyme increased by 100–150% as a result of sucrose feeding. However, glycogen content and the activities of glycogen synthase and phosphorylase in liver remained unaltered in these animals. The plasma levels of triacylglycerols and insulin in the rats fed on vanadate supplemented sucrose diet were 65% and 85% less, respectively as compared to rats on sucrose diet without vanadate. The concentrations of glucose and cholesterol in plasma and the activities of lipogenic enzymes in liver did not show any elevation in sucrose fed rats when supplemented with vanadate. These data indicate that the sucrose diet-induced metabolic aberrations can be prevented by the insulin-mimetic agent, vanadate.     

Effect of Rebaudioside A, a diterpenoid on glucose homeostasis in STZ-induced diabetic rats

Rebaudioside A (Reb A), a major constituent of Stevia rebaudiana, was recently proposed as an insulinotropic agent. The aim of this investigation was to evaluate the antihyperglycemic effect of Reb A on the activities of hepatic enzymes of carbohydrate metabolism in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in adult male Albino Wistar rats, weighing 180-200 g, by a single intraperitoneal injection at a dose of STZ (40 mg/kg body weight). Diabetic rats showed significant (P<0.05) increase in the levels of plasma glucose and glycosylated hemoglobin and significant (P<0.05) decrease in the levels of plasma insulin and hemoglobin. Activities of gluconeogenic enzymes such as glucose-6-phosphatase and fructose-1,6-bisphosphatase were significantly (P<0.05) increased while hexokinase and glucose-6-phosphate dehydrogenase were significantly (P<0.05) decreased in the liver along with glycogen. Oral treatment with Reb A to diabetic rats significantly (P<0.05) decreased blood glucose and reversed these hepatic carbohydrate metabolizing enzymes in a significant manner. Histopathology changes of pancreas confirmed the protective effects of Reb A in diabetic rats. Thus, the results show that Reb A possesses an antihyperglycemic activity and provide evidence for its traditional usage in the control of diabetes.