scholarly journals Hypoglycaemic activity of Coccinia indica and Momordica charantia in diabetic rats: depression of the hepatic gluconeogenic enzymes glucose-6-phosphatase and fructose-1,6-bisphosphatase and elevation of both liver and red-cell shunt enzyme glucose-6-phosphate dehydrogenase

1993 ◽  
Vol 292 (1) ◽  
pp. 267-270 ◽  
Author(s):  
B A Shibib ◽  
L A Khan ◽  
R Rahman
Keyword(s):  
Blood Glucose ◽  
Diabetic Rats ◽  
Momordica Charantia ◽  
Red Cell ◽  
Gluconeogenic Enzymes ◽  
Hepatic Glucose ◽  
Fructose 1,6 Bisphosphatase ◽  
Streptozotocin Diabetic Rats ◽  
Coccinia Indica ◽  
Glucose 6 Phosphate Dehydrogenase

Coccinia indica leaves were extracted with 60% ethanol, solvents were evaporated and the residue was suspended in water. This suspension was administered orally at a dose of 200 mg/kg body wt. after 18 h of fasting to normal fed and streptozotocin-induced male diabetic rats (180-250 g). After 90 min the rats were killed, and blood-glucose, hepatic glucose-6-phosphatase, fructose-1,6-bisphosphatase and glucose-6-phosphate dehydrogenase (G6PDH) and red-cell G6PDH were assayed. Blood sugar was depressed by 23% (P < 0.01) and 27% (P < 0.001) in the normal fed and streptozotocin-diabetic rats respectively compared with controls which were given distilled water. Hepatic glucose-6-phosphatase and fructose-1,6-bisphosphatase activities were depressed by 32% (P < 0.001) 30% (P < 0.05) respectively in the streptozotocin-diabetic rats, compared with 19% (P < 0.02) and 20% (P < 0.01) depression in the normal fed controls, whereas both the red-cell and hepatic G6PDH activities were found to be elevated by feeding the extract in the streptozotocin-diabetic and in the normal fed controls. Similar results were obtained with the 95%-ethanolic extract of Momordica charantia. Taken together, these results indicate that Coccinia indica and Momordica charantia extracts lowered blood glucose by depressing its synthesis, on the one hand through depression of the key gluconeogenic enzymes glucose-6-phosphatase and fructose-1,6-bisphosphatase and on the other by enhancing glucose oxidation by the shunt pathway through activation of its principal enzyme G6PDH.

Improvement in cardiac dysfunction in streptozotocin-induced diabetic rats following chronic oral administration of bis(maltolato)oxovanadium(IV)

1993 ◽  
Vol 71 (3-4) ◽  
pp. 270-276 ◽  
Author(s):  
Violet G. Yuen ◽  
Chris Orvig ◽  
Katherine H. Thompson ◽  
John H. McNeill
Keyword(s):  
Blood Glucose ◽  
Heart Function ◽  
Myocardial Dysfunction ◽  
Plasma Lipid ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Vanadium Complex ◽  
Significant Correction ◽  
Streptozotocin Diabetic Rats

Decreased cardiac function in streptozotocin-diabetic rats has been used as a model of diabetes-induced cardiomyopathy, which is a secondary complication in diabetic patients. The present study was designed to evaluate the therapeutic effect of a new organic vanadium complex, bis(maltolato)oxovanadium(IV), (BMOV), in improving heart function in streptozotocin-diabetic rats. There were four groups of male, Wistar rats: control (C), control treated (CT), diabetic (D), and diabetic treated (DT). Treatment consisted of BMOV, 0.5 mg/mL (1.8 mM) for the first 3 weeks and 0.75 mg/mL (2.4 mM) for the next 22 weeks, in the drinking water of rats allowed ad libitum access to food and water. BMOV lowered blood glucose to < 9 mM in 70% of DT animals without any increase in plasma insulin levels, and mean blood glucose and plasma lipid levels were significantly lower in DT vs. D rats. Tissue vanadium levels were measured in plasma, bone, kidney, liver, muscle, and fat of BMOV-treated rats. Plasma vanadium levels averaged 0.84 ± 0.07 μg/mL (16.8 μM) in CT rats and 0.76 ± 0.05 μg/mL (15.2 μM) in DT animals. The highest vanadium levels at termination of this chronic feeding study were in bone, 18.3 ± 3.0 μg/g (0.37 μmol/g) in CT and 26.4 ± 2.6 μg/g (0.53 μmol/g) in DT rats, with intermediate levels in kidney and liver, and low, but detectable levels in muscle and fat. There were no deaths in either the CT or DT group, and no overt signs of vanadium toxicity were present. Tissue vanadium levels were not correlated with the glucose-lowering effect. Isolated working heart parameters of left ventricular developed pressure (LVDP) and rate of pressure development (+dP/dT, and −dP/dT) indicated that BMOV treatment resulted in significant correction of the heart dysfunction associated with streptozotocin-induced diabetes in rat.Key words: bis(maltolato)oxovanadium(IV), vanadium, diabetes, streptozotocin, myocardial dysfunction.

scholarly journals P0950EFFECT OF THYROID HORMONE TREATMENT ON RENAL REABSORPTION OF GLUCOSE IN ALLOXAN-INDUCED DIABETIC RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Gireesh Dayma
Keyword(s):  
Blood Glucose ◽  
Thyroid Hormone ◽  
Glucose Homeostasis ◽  
Hepatic Glucose Production ◽  
Liver Perfusion ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Renal Expression

Abstract Background and Aims The thyroid hormone (TH) plays an important role in glucose metabolism. Recently, we showed that the TH improves glycemia control by decreasing cytokines expression in the adipose tissue and skeletal muscle of alloxan-induced diabetic rats, which were also shown to present primary hypothyroidism. In this context, this study aims to investigate whether the chronic treatment of diabetic rats with T3 could affect other tissues that are involved in the control of glucose homeostasis, as the liver and kidney. Method Adult male Wistar rats were divided into nondiabetic, diabetic, and diabetic treated with T3 (1.5 ?g/100 g BW for 4 weeks). Diabetes was induced by alloxan monohydrate (150 mg/kg, BW, i.p.). Animals showing fasting blood glucose levels greater than 250 mg/dL were selected for the study. Results After treatment, we measured the blood glucose, serum T3, T4, TSH, and insulin concentration, hepatic glucose production by liver perfusion, liver PEPCK, GAPDH, and pAKT expression, as well as urine glucose concentration and renal expression of SGLT2 and GLUT2. T3 reduced blood glucose, hepatic glucose production, liver PEPCK, GAPDH, and pAKT content and the renal expression of SGLT2 and increased glycosuria. Conclusion Results suggest that the decreased hepatic glucose output and increased glucose excretion induced by T3 treatment are important mechanisms that contribute to reduce serum concentration of glucose, accounting for the improvement of glucose homeostasis control in diabetic rats.

Effect of Garlic Oil on the Levels of Various Enzymes in the Serum and Tissue of Streptozotocin Diabetic Rats

2001 ◽  
Vol 21 (1) ◽  
pp. 19-24 ◽  
Author(s):  
O. C. Ohaeri
Keyword(s):  
Serum Amylase ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Red Cell ◽  
Alkaline Phosphatases ◽  
Garlic Oil ◽  
Acid And Alkaline Phosphatase ◽  
Liver And Kidney ◽  
Streptozotocin Diabetic Rats ◽  
Aspartate Transferase

Levels of red cell, serum acid, and alkaline phosphatases, serum amylase, alanine and aspartate transferase and bilirubin were examined in streptozotocin-induced diabetic rats treated with garlic oil and compared with the corresponding levels in diabetic control rats, normal rats and normal rats on garlic oil. Values of tissue amylase and total protein were also assessed from the pancreas, liver, and kidney. Treatment of diabetic rats with garlic oil significantly decreased the red cell phosphatase (p<0.01), serum acid and alkaline phosphatase (p<0.001) when compared to diabetic control rats. Serum alanine and asparate transferases were significantly (p<0.001) decreased as well as serum amylase (p<0.002) in garlic oil treated diabetic rats as compared with diabetic control rats. When treated with garlic oil, however, diabetic and normal rats showed significant increase (p<0.05) in the amylase levels of the pancrease, liver, and kidney.

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