Effect of cogent db,a herbal drug,on plasma insulin and hepatic enzymes of glucose metabolism in experimental diabetes

Aims: The present study was designed to investigate the effect of cogent db, a polyherbal drug on blood glucose, plasma insulin and the activities of hepatic glucose metabolic enzymes in alloxan-induced diabetic rats.
Methods: Male Wistar rats body weight of 180–200 g (six normal and 18 diabetic rats) were used in this study. The rats were divided into four groups after the induction of alloxan diabetes. In the experiment, six rats were used in each group: Group 1, normal rats given 2 ml of saline; Group 2, diabetic control rats given 2 ml of saline; Group 3, diabetic rats given aqueous solution of cogent db (0.45 g/body kg weight); and Group 4, diabetic rats given aqueous solution of glibenclamide (600 µg/kg body weight). The treatment was given for 40 days. After the treatment, fasting blood glucose, plasma insulin, urine sugar and the activities of hepatic glucose metabolic enzymes were determined in normal and experimental animals.
Results: Treatment with cogent db resulted in a significant reduction in blood glucose and the activities of glucose-6-phosphatase and fructose-1,6-bisphosphatase in the liver, whereas the level of plasma insulin and hepatic hexokinase activity were significantly increased in alloxan-diabetic rats.
Conclusions: The present investigation suggests that cogent db controls the blood glucose level by increasing glycolysis and decreasing gluconeogenesis with a lower demand of pancreatic insulin than in untreated rats. This is possible because it regulates the activities of hepatic glucose metabolic enzymes.     

Change in the lipid profile, lipogenic and related enzymes in the livers of experimental diabetic rats: effect of insulin and vanadate

Administration of sodium orthovanadate to diabetic animals exhibits insulin-like effects and has been effective in the reversal of biochemical complications. This study evaluates the effect of sodium orthovanadate (0.6 mg/ml) treatment for 21 days on the hepatic glucose homeostasis and lipid metabolism in alloxan diabetic rats. The activities of two lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme; and related enzymes, hexokinase and glucose-6-phosphatase were measured in the liver cytosolic fractions of diabetic rats and diabetic rats treated separately with insulin and sodium orthovanadate. The total lipids, triglycerides and cholesterol levels were estimated in the livers of the diabetic and the treated rats. The activities of both the lipogenic enzymes and hexokinase isozymes were significantly decreased, whereas the activity of glucose-6-phosphatase was significantly increased in the diabetic liver. During diabetes, the levels of total lipids and triglycerides increased significantly with a decrease in the cholesterol levels in the liver. Insulin and vanadate were able to restore the altered enzyme activities to almost control levels. Both insulin and vanadate were found to partially restore the altered levels of total lipids, triglycerides and cholesterol in the livers of diabetic rats. The results indicate that vanadate administration to diabetic animals normalizes blood glucose and causes marked improvement of altered lipid metabolism during diabetes. The present study and earlier reports suggest the possible use of vanadate as insulin replacement in the therapy of diabetes when administered at pharmacological doses.     

Antidiabetic effect of diasulin, a herbal drug, on blood glucose, plasma insulin and hepatic enzymes of glucose metabolism in hyperglycaemic rats

AIM: The present study was designed to investigate the effect of diasulin, a polyherbal drug, on blood glucose, plasma insulin and the activities of hepatic glucose metabolic enzymes in alloxan-induced diabetic rats. METHODS: Male Wistar rats, body weight of 180-200 g (12 normal and 30 diabetic rats), were used in this study. The rats were divided into seven groups after the induction of alloxan diabetes. In the experiment, six rats were used in each group. Group 1: normal rats given 2 ml of saline; group 2: normal rats given aqueous solution of diasulin (0.20 g/kg of body weight); group 3: diabetic control rats given 2 ml of saline; group 4: diabetic rats given aqueous solution of diasulin (0.05 g/kg of body weight); group 5: diabetic rats given aqueous solution of diasulin (0.10 g/kg of body weight); group 6: diabetic rats given aqueous solution of diasulin (0.20 g/kg of body weight) and group 7: diabetic rats given aqueous solution of glibenclamide (600 micro g/kg of body weight). The treatment was given for 30 days. After the treatment, fasting blood glucose, plasma insulin, urine sugar and the activities of hepatic glucose metabolic enzymes were determined in normal and experimental animals. RESULTS: Treatment with diasulin resulted in a significant reduction in blood glucose, glycosylated haemoglobin and an increase in plasma insulin and total haemoglobin and a significant improvement in glucose tolerance. Diasulin also resulted in a significant reduction in the activities of glucose-6-phosphatase and fructose-1,6-bisphosphatase in the liver, whereas the level of plasma insulin and hepatic hexokinase activity was significantly increased in alloxan diabetic rats. CONCLUSIONS: The present investigation suggests that diasulin, a polyherbal drug, controls the blood glucose level by increasing glycolysis and decreasing gluconeogenesis with a lower demand of pancreatic insulin than in untreated rats. This is possible, because it regulates the activities of hepatic glucose metabolic enzymes.     

Changes in metabolism of rat kidney and liver caused by experimental diabetes and by dietary sucrose

Summary Two groups of rats were fed diets in which the carbohydrate component was either starch or sucrose. A third group was fed on a stock diet. Half of the animals in each group were made diabetic by injection of either streptozotocin, in two of the groups, or alloxan, in the third group.Both diabetes and sucrose-feeding increased renal gluconeogenesis as indicated by increased activities of fructose-1,6-diphosphatase and glucose-6-phosphatase. Sucrose-feeding increased fatty acid synthesis both in the liver and kidney. However, the effect of diabetes on fatty acid synthesis was different at the two tissue sites. Diabetes, whether induced by streptozotocin or alloxan, decreased fatty acid synthesis in the liver but increased the rate in the kidney. The latter response was obtained for each diet but was additive with the effect of sucrose.We conclude that the effect of diabetes on renal lipid metabolism may reflect, in part, the accelerated glucose flux. The response to both diabetes and sucrose-feeding is also possibly associated with the increased lipid required for the membrane synthesis reported previously.     

Effect of Gymnema montanum leaves on serum and tissue lipids in alloxan diabetic rats

The effect of Gymnema montanum leaves on alloxan-induced hyperlipidemia was studied in male Wistar rats. Ethanolic extract of G. montanum leaves was administered orally and different doses of the extract on blood glucose, serum and tissue lipids, hexokinase, glucose-6-phosphatase, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and glutathione in alloxan-induced diabetic rats were studied. G. montanum leaf extract (GLEt) at doses of 50, 100, 200 mg/kg body weight for 3 weeks suppressed the elevated blood glucose and lipid levels in diabetic rats. GLEt at 200 mg/kg body weight was found to be comparable to glibenclamide, a reference drug. These data indicate that G. montanum represents an effective antihyperglycemic and antihyperlipidemic adjunct for the treatment of diabetes and a potential source of discovery of new orally active agent for future therapy.     

Androgens activate mitogen-activated protein kinase via epidermal growth factor receptor/insulin-like growth factor 1 receptor in the mouse PC-1 cell line

Insulin replacement is the only effective therapy to manage hyperglycemia in type 1 diabetes mellitus (T1DM). Nevertheless, intensive insulin therapy has inadvertently led to insulin resistance. This study investigates mechanisms involved in the insulin resistance induced by hyperinsulinization. Wistar rats were rendered diabetic by alloxan injection, and 2 weeks later received saline or different doses of neutral protamine Hagedorn insulin (1.5, 3, 6, and 9?U/day) over 7 days. Insulinopenic-untreated rats and 6U- and 9U-treated rats developed insulin resistance, whereas 3U-treated rats revealed the highest grade of insulin sensitivity, but did not achieve good glycemic control as 6U- and 9U-treated rats did. This insulin sensitivity profile was in agreement with glucose transporter 4 expression and translocation in skeletal muscle, and insulin signaling, phosphoenolpyruvate carboxykinase/glucose-6-phosphatase expression and glycogen storage in the liver. Under the expectation that insulin resistance develops in hyperinsulinized diabetic patients, we believe insulin sensitizer approaches should be considered in treating T1DM.     

Rat hepatic microsomal glucose-6-phosphatase protein levels are increased in streptozotocin-induced diabetes

Summary Hepatic microsomal glucose-6-phosphatase activity levels and the hepatic output of glucose are increased in diabetes. We have used protein chemistry and immunological techniques to determine the mechanism by which the activity levels of the glucose-6-phosphatase system are increased in streptozotocin-induced diabetic rats. In the streptozotocin-induced diabetic rats, the activity of the glucose-6-phosphatase enzyme increased four-fold without appreciably altering the transport capacity of the glucose-6-phosphatase system. The solubilized diabetic rat liver glucose-6-phosphatase enzyme appeared to be very similar to the solubilized enzyme from control rat liver microsomes. They exhibit the same Km, are labile at 30 °C, are stabilized by sodium fluoride and they migrate to the same position during density gradient centrifugation. Immunological studies demonstrated that a greater amount of hepatic microsomal glucose-6-phosphatase enzyme protein is present in diabetic rats than in control rats. Thus, we have determined for the first time that increased levels of the glucose-6-phosphatase protein are present in streptozotocin-induced diabetes. The significance of this finding in relation to the regulation of the hepatic microsomal glucose-6-phosphatase system is discussed.     

Hormone-stimulated glucose production from glycogen in hepatocytes from streptozotocin diabetic rats.

The contribution of hormone-stimulated glycogenolysis to hepatic glucose production was studied in hepatocytes from streptozotocin diabetic rats. To this end, the activation of glycogen phosphorylase by glucagon, vasopressin, and the alpha 1-adrenergic agonist phenylephrine was compared in hepatocytes from normal and diabetic rats and related to glycogen content, glucose production, and microsomal glucose-6-phosphatase activity. Streptozotocin-induced diabetes reduced the glycogen content and the amount of total (a + b) phosphorylase in hepatocytes proportionally to the severity of the disease. In cells from severely diabetic rats (group 1), the responsiveness of activation of phosphorylase to the hormones was reduced by about half, consistent with a 45% reduction in total phosphorylase. In addition, the sensitivity of phosphorylase activation to all hormones investigated was decreased by about 1 order of magnitude or more in cells of this group. In hepatocytes from rats with milder diabetes (group 2), maximal phosphorylase activation reached an intermediate value between that of the control group and of group 1. In response to all hormones investigated, group 2 diabetic rat hepatocytes produced less glucose than control rat liver cells, while in group 1 there was no increase in glucose production at all, presumably because glycogen concentration was too low. However, in group 2 diabetic rat hepatocytes, glucagon-stimulated glucose production, unlike phosphorylase activation, did not show decrease sensitivity, presumably because glucose-6-phosphatase activity is increased by diabetes. Our results thus indicate that hormone-stimulated liver glycogenolysis is unlikely to contribute to enhanced glucose production in insulin-deficient diabetes, despite increased glucose-6-phosphatase activity.     

肝脏中糖代谢关键酶作为糖尿病药物靶点的研究进展

葡萄糖激酶、葡萄糖-6-磷酸酶、磷酸烯醇式丙酮酸羧激酶、果糖-1,6-二磷酸酶和糖原磷酸化酶是肝脏中精代谢的关键酶.糖尿病的一个特征就是葡萄糖激酶活性下降和葡萄糖-6-磷酸酶、磷酸烯醇式丙酮酸羧激酶、果糖-1,6-二磷酸酶和糖原磷酸化酶活性的升高.最近的研究都致力于通过激活或抑制这儿种酶来降低血糖并使胰岛素正常分泌.因此这5种酶将有可能是治疗糖尿病的全新靶点.     

Suppression of the hepatic glucose-6-phosphatase system in diabetic rats by vanadate

The effect of oral administration of vanadate on the transport and hydrolytic components of the glucose-6-phosphatase system in liver homogenates from streptozotocin-induced diabetic rats was examined. Blood glucose was normalized in diabetic rats receiving 0.8 mg/ml vanadate but a catabolic effect was observed on body and liver weight. Significant changes in the coupled reactions for glucose-6-phosphate transport by T1 and hydrolysis by the enzyme were noted. The dramatic elevation in the maximal velocity of glucose-6-phosphatase brought about by diabetes was suppressed by vanadate administration. As a result, the relationship between T1 and the enzyme returned to the normal range. It is concluded that the suppression of glucose-6-phosphate hydrolysis in diabetes may contribute to the normalizing effect of vanadate on blood glucose.     

Antidiabetic, hypolipidemic and histopathological analysis of Dillenia indica (L.) leaves extract on alloxan induced diabetic rats

ObjectiveTo investigate antidiabetic, hypolipidemic histopathological analysis of Dillenia indica (D. indica) methanolic leaves (DIME) extract in alloxan induced diabetic rat by administering oral doses (250 and 500 mg/kg body weight).MethodsBlood glucose levels were measured using blood glucose test strips with elegance glucometer on weekly intervals till the end of study (i.e. 3 weeks). Other parameters e.g. liver profile, renal profile and total lipid levels were determined in normal and alloxan induced diabetic rats after oral administration of the extract for 21 days. Histopathological changes in diabetic rat organs (pancreas, liver and kidney) were also observed after extract treatment.ResultsDaily oral administration DIME (250 and 500 mg/kg body weight) and glibenclamide (10 mg/kg) showed beneficial effects on blood glucose level (P < 0.001) as well as improving kidney, liver functions and hyperlipidaemia due to diabetes. The extract treatment also showed to enhanced serum insulin level and body weight of diabetic rats as compared to diabetic control group. Furthermore, the extract has a favorable effect on the histopathological changes of the pancreas, liver and kidney in alloxan induced diabetes.ConclusionsD. indica possess antidiabetic property as well improve body weight, liver profile, renal profile and total lipid levels. DIME has also favorable effect to inhibit the histopathological changes of the pancreas and kidney in alloxan induced diabetes.     

Hypoglycemic effect of Costus pictus D. Don on alloxan induced type 2 diabetes mellitus in albino rats

ObjectiveTo demonstrate the effect of aqueous extract of Costus pictus (C. pictus) leaves on blood glucose, lipid profile and liver antioxidant enzymes and lipid peroxidation in alloxan induced diabetic rats.MethodsAqueous extract of C. pictus (AECP) leaves was administered orally for 30 days and its effect on blood glucose, lipid profile, hepatic marker enzymes such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), serum urea, creatinine, protein and albumin content and liver antioxidant enzymes such as catalase, peroxidase, superoxide dismutase and lipid peroxidation in alloxan induced diabetic rats were examined.ResultsOral administration of aqueous extract of C. pictus leaves to diabetic rats for 30 days significantly reduced the levels of blood glucose, lipid profile, lipid peroxidation, liver marker enzymes, urea, creatinine and increased the levels of antioxidant enzymes.ConclusionsThe aqueous extract of C. pictus leaves controls the blood glucose level, improves lipid metabolism and prevents diabetic complications associated with lipid peroxidation and also maintains the antioxidant enzymes in experimental diabetic rats. Therefore, it can be recommeded for the prevention of diabetes mellitus.     

Global gene expression analysis in liver of obese diabetic db/db mice treated with metformin

Aims/hypothesis Metformin is widely used as a hypoglycaemic reagent for type 2 diabetes. While the reduction of hepatic gluconeogenesis is thought to be a key effect, the detailed molecular mechanism of action of metformin remains to be elucidated. To gain insight into this, we performed a global gene expression profiling study.Materials and methods We performed DNA microarray analysis to study global gene expression in the livers of obese diabetic db/db mice 2 h after a single administration of metformin (400 mg/kg).Results This analysis identified 14 genes that showed at least a 1.5-fold difference in expression following metformin treatment, including a reduction of glucose-6-phosphatase gene expression. The mRNA levels of glucose-6-phosphatase showed one of the best correlations with blood glucose levels among 12,000 genes. Enzymatic activity of glucose-6-phosphatase was also reduced in metformin-treated liver. Moreover, intensive analysis of the expression profile revealed that metformin effected significant alterations in gene expression across at least ten metabolic pathways, including those involved in glycolysis-gluconeogenesis, fatty acid metabolism and amino acid metabolism.Conclusions/interpretation These results suggest that reduction of glucose-6-phosphatase activity, as well as suppression of mRNA expression levels of this gene, in liver is of prime importance for controlling blood glucose levels in vivo, at least at early time points after metformin treatment. Our results also suggest that metformin not only affects expression of specific genes, but also alters the expression level of multiple genes linked to the metabolic pathways involved in glucose and lipid metabolism in the liver.Electronic Supplementary Material Supplementary material is available in the online version of this article at     

Insulin and glucagon releasing activity of coleonol (forskolin) and its effect on blood glucose level in normal and alloxan diabetic rats

Summary Colenol, a diterpenoid isolated from the roots ofColeus forskohlii stimulates the release of insulin and glucagon from the islets bothin vitro andin vivo. Coleonol-stimulated release of glucagon from isletsin vitro is much more pronounced as compared to that of insulin. Glucose concentration of 5.6 mM in the medium is required for the coleonol stimulation of insulin release. Feeding of coleonol to alloxan diabetic rats cause 36.5% increase in blood glucose level as compared to alloxan diabetic control. Oral feeding of coleonol for 7 days to normal rats causes increase in blood glucose, serum insulin, glucagon and free fatty acid levels with corresponding increase in glucose-6-phosphatase activity and depletion of liver glycogen. Predominant stimulation of A-cells by coleonol is suggested for the above effects. C.D.R.I. Communication n ^o 4646.     

Ishige okamurae ameliorates hyperglycemia and insulin resistance in C57BL/KsJ-db/db mice

We investigated the effect of Ishige okamurae extract on blood glucose level and insulin resistance in C57BL/-KsJ-db/db mice. We administered a standard AIN-93G diet with or without IOE to the animals for 6 weeks. After 6 weeks, blood glucose level was improved and blood glycosylated hemoglobin levels were lowered in sample group mice as compared to those in the diabetic control group mice. Hyperinsulinemia was reduced in the I. okamurae extract group mice with type 2 diabetes. With regard to hepatic glucose metabolic enzyme activities, glucokinase activity was enhanced in the IOE group mice, while glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities in the IOE group mice were significantly lowered than those in the diabetic control group mice. In addition, the hepatic glycogen content was elevated in the IOE group as compared to that in the diabetic control group. The homeostatic index of insulin resistance was lower in the I. okamurae extract group mice than in the diabetic control group mice. These results suggest that a dietary supplement of I. okamurae extract lowers the blood glucose level by altering the hepatic glucose metabolic enzyme activities and improves insulin resistance.     

Adaptation in enzyme (metabolic) pathways to obesity, carbohydrate diet and to the occurrence of NIDDM in male and female SHR/N-cp rats.

Twenty-four male (12 obese and 12 lean) and 21 female (11 obese and 10 lean) SHR/N-cp rats were fed a diet containing either 54% sucrose or starch for periods of 3-4 months. Rats were killed after a 14-16 h fast and liver enzyme activities were determined in both sex groups. Liver glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FBPase), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), malic enzyme (ME), phosphofructokinase (PFK), glucokinase (GK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels (per total liver capacity) were significantly affected by phenotype (obese > lean). Arginase and ornithine transcarbamylase levels were analysed only in male rats and were found to be elevated in obese rats as compared to lean littermates. Some of the above changes in enzyme levels were exaggerated by sucrose feeding but not the changes in FBPase, PEPCK, ME and GK (in both sexes) plus AST, arginase and arginine synthase activities in male rats and ALT levels in female rats. Results from SHR/N-cp rats published in this paper were compared to results obtained from LA/N-cp rats published previously. Comparison of the non-diabetic obese LA/N-cp with the diabetic obese SHR/N-cp male shows a greater excess in lipogenic capacity of the liver in the LA/N-cp male rat. The SHR/N-cp obese female also shows a greater liver lipogenic capacity as compared with the obese male SHR/N-cp rat. The results suggest that an adaptation of excessive lipogenesis in the liver of obese rats may be an anti-diabetogenic adaptation resulting in increased glucose conversion to lipids, thus reducing blood glucose levels.     

Direct regulation of glucose and not insulin on hepatic hexose-6-phosphate dehydrogenase and 11β-hydroxysteroid dehydrogenase type 1

Abnormal hepatic gluconeogenesis contributes significantly to both fasting and non-fasting hyperglycemia of patients with type 2 diabetes. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates the key hepatic gluconeogenic enzymes including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) through the amplification of glucocorticoid receptor (GR) - mediated tissue glucocorticoid action, and is crucially dependent on hexose-6-phosphate dehydrogenase (H6PDH) - generating NADPH system. Here, we observed that compared with fasting state, H6PDH and 11β-HSD1 expression in livers were all increased under non-fasting state in both normal and diabetic rats, and the non-fasting diabetic group was the highest among the four experimental groups. Moreover, incubation of primary hepatocytes with increasing glucose caused dose-dependent increases in H6PDH, 11β-HSD1, GR, PEPCK and G6Pase expression. Also, glucose-6-phosphate (G6P) had a positive regulation on H6PDH and 11β-HSD1 in hepatocytes. In addition, primary hepatocytes treated with different doses of insulin in high glucose induced alteration of H6PDH and 11β-HSD1 while in low glucose there was no significant effect. These findings suggest that glucose instead of insulin directly regulates H6PDH and 11β-HSD1 and suppression of the two enzymes could be considered as an effective target for the treatment of type 2 diabetes.     

Experimental evidence for the use of CCR2 antagonists in the treatment of type 2 diabetes

ObjectiveCCR2 inhibition has produced promising experimental and clinical anti-hyperglycemic effects. These results support the thesis that insulin resistance and Type 2 diabetes (T2D) are associated with chronic unresolved inflammation. The aim of this study was to provide a broad analysis of the various physiological changes occurring in mouse models of T2D in connection with pharmacological CCR2 inhibition.Materials/MethodsA mouse-active chemical analogue of the clinical candidate CCX140-B was tested in diet-induced obese (DIO) mice and db/db mice. Measurements included: adipose tissue inflammatory macrophage counts; peripheral blood glucose levels at steady-state and after glucose and insulin challenges; peripheral blood insulin and adiponectin levels; 24-h urine output and urinary glucose levels; pancreatic islet number and size; hepatic triglyceride and glycogen content; and hepatic glucose-6-phosphatase levels.ResultsIn DIO mice, the CCR2 antagonist completely blocked the recruitment of inflammatory macrophages to visceral adipose tissue. The mice exhibited reduced hyperglycemia and insulinemia, improved insulin sensitivity, increased circulating adiponectin levels, decreased pancreatic islet size and increased islet number. It also reduced urine output, glucose excretion, hepatic glycogen and triglyceride content and glucose 6-phosphatase levels. Similar effects were observed in the db/db diabetic mice.ConclusionsThese data indicate that pharmacological inhibition of CCR2 in models of T2D can reduce inflammation in adipose tissue, alter hepatic metabolism and ameliorate multiple diabetic parameters. These mechanisms may contribute to the promising anti-diabetic effects seen in humans with at least one CCR2 antagonist.     

Effects of hydro-ethanol extract of Citrullus colocynthis on blood glucose levels and pathology of organs in alloxan-induced diabetic rats

Objective

To evaluated the differential effects of ethanol extraction of Citrullus colocynthis (C. colocynthis) on the blood glucose concentration and pathology of pancreas, liver, lungs, kidney and gastrointestinal tract in the alloxan induced diabetes in rats.

Methods

Diabetes mellitus was induced in 20 adult female Albino rats, using intraperitoneal injection of 120 mg/kg alloxan. The diabetic rats were randomly assigned into two equal groups. The first group was treated with the extract of C. colocynthis seed (300 mg/kg) and the rats of the second group, as an untreated diabetic group, received ordinary diet. Ten non diabetic rats remained as a normal control group.

Results

The results of this study indicate that C. colocynthis was able to reduce blood glucose significantly compared with the control diabetic group (P<0.05). Histopathologically, alloxan resulted in severe necrotic changes in the pancreatic islets, especially in the central area of the islets. Tissue sections of the pancreas in the treated rats demonstrated enhanced regeneration of B cells and increased size of pancreatic islets. Liver of the treated diabetic rats revealed significant improvement of the hepatic tissue compared to those of the untreated diabetic rats.

Conclusions

The present study indicated a significant anti-hyperglycemic effect of C. colocynthis seed and supported its traditional usage in treatment of diabetes mellitus.     

Effects of swimming training at the intensity equivalent to aerobic/anaerobic metabolic transition in alloxan diabetic rats

The present study was designed to determine the exercise intensity equivalent to the metabolic aerobic/anaerobic transition of alloxan diabetic rats, through lactate minimum test (LMT), and to evaluate the effects of swimming exercise at this intensity (LM) on the glucose and protein metabolism of these animals. Adult male Wistar rats received alloxan (SD, alloxan-injected rats that remained sedentary) intravenously (30 mg kg(-1) body weight) for diabetes induction. As controls (SC, vehicle-injected rats that remained sedentary), vehicle-injected rats were utilized. Two weeks later, the animals were submitted to oral glucose tolerance test (oGTT) and LMT. After the tests, some of the animals were submitted to swimming exercise training [TC (vehicle-injected rats that performed a 6-week exercise program) and TD (alloxan-injected rats that performed a 6-week exercise program)] for 1 h day(-1), 5 days week(-1), with an overload equivalent to LM determined by LMT, for 6 weeks. At the end of the experiment, the animals were submitted to a second LMT and oGTT, and blood and skeletal muscle assessments (protein synthesis and degradation in the isolated soleus muscle) were made. The overload equivalent to LM at the beginning of the experiment was lower in the SD group than in the SC group. After training, the overload equivalent to LM was higher in the TC and TD groups than in the SC and SD groups. The blood glucose of TD rats during oGTT was lower than that of SD rats. Protein degradation was higher in the SD group than in other groups. We conclude that LMT was sensitive to metabolic and physiologic alterations caused by uncontrolled diabetes. Training at LM intensity improved aerobic condition and the glucose and protein metabolism of alloxan diabetic rats.