31
Another portion of wet liver tissue was used for the estimation of glycogen content.32 The TCA cycle enzymes were also assayed. Isocitrate dehydrogenase enzyme activity was assayed according to the method of Bell and Baron.33 α-Ketoglutarate dehydrogenase enzyme activity was estimated selleck according to the method of Reed and Mukherjee.34 Succinate dehydrogenase enzyme activity was estimated according to the method of Slater and Bonner.35 Malate dehydrogenase activity of malate dehydrogenase was assayed by the method of Mehler et al.36 The results were expressed as mean ± S.E.M of six rats per group and statistical significance was evaluated by one way analysis of variance (ANOVA) using SPSS (version 16.0) program followed by LSD. Table 1 shows the qualitative analysis of phytochemicals present in the ethanolic extract of Mengkudu fruits. From preliminary secondary metabolites screening, it was found that the extract showed a positive response for the presence of flavonoids, alkaloids, glycosides, saponins, proteins, triterpenoids and phenols. Table 2 and Fig. 1 portray the effect of oral administration of MFE on blood glucose, Hemoglobin, glycosylated hemoglobin, plasma insulin, and C-peptide levels in experimental groups
of animals. There was a significant elevation in the levels of blood glucose and glycosylated hemoglobin and concomitant fall in Hb of STZ induced diabetic rats as compared Selinexor supplier with control group of rats. Upon treatment with MFE as well as gliclazide for 30 days, diabetic rats showed a significant decrease in the levels of blood glucose and glycosylated hemoglobin, and proportionate rise in Hb, which were comparable with control group of rats. Moreover, the significantly diminished plasma very insulin and C-peptide levels of diabetic rats were improved substantially to near normal level by the administration with MFE as well as gliclazide. Tables 3 and 4 depict the outcome of
MFE supplementation on the activities of hexokinase, pyruvate kinase, LDH, glucose-6-phosphatase, fructose-1, 6-bisphosphatase and glucose-6-phosphate dehydrogenase in liver and kidney tissues of control and experimental groups of rats. The enzymes activities were altered in liver and kidney tissues of STZ induced diabetic rats. Upon treatment with MFE as well as gliclazide for 30 days, diabetic rats improved from the altered enzyme activities to near normalcy in liver and kidney tissues. Tables 5 and 6 represents the activities of TCA cycle key enzymes in liver and kidney tissues of control and experimental groups of rats. The liver and kidney tissues of diabetic rats showed momentous depleted activities of isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase.