Comparative Evaluation of the Antidiabetic Effects of Different Parts ofCassia fistulaLinn, a Southeast Asian Plant

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Abstract

The hypoglycemic effect of the methanolic and aqueous extracts of whole parts of Cassia fistulain both normoglycemic and streptozotocin-nictotinamide induced Type 2 diabetic rats were investigated. Acute toxicity, oral glucose tolerance test and glucose uptake in isolated rat hemidiaphragm were performed in normal rats. Diabetes was induced in Sprague Dawley rats by the administration of streptozotocin-nictotinamide (50, 110 mg/kg b.w., resp.) intraperitoneally. Different extracts of Cassiawas administered to diabetic rats at 250 and 500 mg/kg doses for 21 days. Biochemical parameters like blood glucose, insulin, glycosylated hemoglobin, lipid profile, and serum marker enzymes were determined. The methanolic extract of the bark and leaves were show more effective in causing hypoglycemia in normoglycemic rats. Diabetic rats showed increased levels of glycosylated hemoglobin, reduced levels of plasma insulin, were significantly reverted to near normal after oral administration of the bark and leaf methanolic extracts. Glucose uptake studies in isolated rat hemidiaphragm have shown enhanced peripheral utilization of glucose. Chronic treatment of Cassiaremarkably restored the normal status of the histopathological changes observed in the selected tissues. Dose dependent anti-diabetic effects with the cohorts receiving the methanolic extract of bark followed by leaves of Cassiawas revealed.

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Medicinal plants of India with anti-diabetic potential.

J.K Grover, S. Yadav, V Vats (2002)

Since ancient times, plants have been an exemplary source of medicine. Ayurveda and other Indian literature mention the use of plants in treatment of various human ailments. India has about 45000 plant species and among them, several thousands have been claimed to possess medicinal properties. Research conducted in last few decades on plants mentioned in ancient literature or used traditionally for diabetes have shown anti-diabetic property. The present paper reviews 45 such plants and their products (active, natural principles and crude extracts) that have been mentioned/used in the Indian traditional system of medicine and have shown experimental or clinical anti-diabetic activity. Indian plants which are most effective and the most commonly studied in relation to diabetes and their complications are: Allium cepa, Allium sativum, Aloe vera, Cajanus cajan, Coccinia indica, Caesalpinia bonducella, Ficus bengalenesis, Gymnema sylvestre, Momordica charantia, Ocimum sanctum, Pterocarpus marsupium, Swertia chirayita, Syzigium cumini, Tinospora cordifolia and Trigonella foenum graecum. Among these we have evaluated M. charantia, Eugenia jambolana, Mucuna pruriens, T. cordifolia, T. foenum graecum, O. sanctum, P. marsupium, Murraya koeingii and Brassica juncea. All plants have shown varying degree of hypoglycemic and anti-hyperglycemic activity.

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Pathogenesis of NIDDM. A balanced overview.

R DeFronzo, R C Bonadonna, E Ferrannini (1992)

Non-insulin-dependent diabetes mellitus (NIDDM) results from an imbalance between insulin sensitivity and insulin secretion. Both longitudinal and cross-sectional studies have demonstrated that the earliest detectable abnormality in NIDDM is an impairment in the body's ability to respond to insulin. Because the pancreas is able to appropriately augment its secretion of insulin to offset the insulin resistance, glucose tolerance remains normal. With time, however, the beta-cell fails to maintain its high rate of insulin secretion and the relative insulinopenia (i.e., relative to the degree of insulin resistance) leads to the development of impaired glucose tolerance and eventually overt diabetes mellitus. The cause of pancreatic "exhaustion" remains unknown but may be related to the effect of glucose toxicity in a genetically predisposed beta-cell. Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered beta-cell function in NIDDM. Insulin resistance in NIDDM involves both hepatic and peripheral, muscle, tissues. In the postabsorptive state hepatic glucose output is normal or increased, despite the presence of fasting hyperinsulinemia, whereas the efficiency of tissue glucose uptake is reduced. In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. The accelerated rate of hepatic glucose output is due entirely to augmented gluconeogenesis. In muscle many cellular defects in insulin action have been described including impaired insulin-receptor tyrosine kinase activity, diminished glucose transport, and reduced glycogen synthase and pyruvate dehydrogenase. The abnormalities account for disturbances in the two major intracellular pathways of glucose disposal, glycogen synthesis, and glucose oxidation. In the earliest stages of NIDDM, the major defect involves the inability of insulin to promote glucose uptake and storage as glycogen. Other potential mechanisms that have been put forward to explain the insulin resistance, include increased lipid oxidation, altered skeletal muscle capillary density/fiber type/blood flow, impaired insulin transport across the vascular endothelium, increased amylin, calcitonin gene-related peptide levels, and glucose toxicity.