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      Enhanced glycemic control, pancreas protective, antioxidant and hepatoprotective effects by umbelliferon-α-D-glucopyranosyl-(2 I → 1 II)-α-D-glucopyranoside in streptozotocin induced diabetic rats

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          Abstract

          Objective

          The objective of the present study was to evaluate the effect of umbelliferon-α-D-glucopyranosyl-(2I → 1II)-α-D-glucopyranoside (UFD) from Aegle marmelos Corr. on serum glucose, lipid profile and free radical scavenging activity in normal and STZ (streptozotocin) induced diabetic rats.

          Materials and methods

          Diabetes was induced by single interperitoneal injecting of streptozotocin (60 mg/kg, i.p.) in the rats. All the rats were divided into following groups; I - nondiabeteic, II - nondiabetic + UFD (40 mg/kg, p.o.), III - diabetic control, IV - UFD (10 mg/kg, p.o.), V - UFD (20 mg/kg, p.o.), VI - UFD (40 mg/kg) and VII - glibenclamide (10 mg/kg, p.o.). Serum glucose level and body weight were determined periodically. Biochemical parameter, antioxidant enzyme and histopathology study were performed on the day 28. Oral glucose tolerance test study was performed to identify the glucose utilization capacity.

          Results

          All the doses of UFD and glibenclamide decrease the level of serum glucose, glycated hemoglobin, glucose-6-phosphatase, fructose-1-6-biphosphate and increased the level of plasma insulin, hexokinase. The UFD doses also showed effects on antioxidant enzymes viz. superoxide dismutase, catalase and glutathione peroxidase which were significantly increased and the level of malonaldehyde was markedly decreased. Histologically study, focal necrosis, deposition of fats, increased the size of the intercalated disc were observed in the diabetic rat liver, kidney, heart and pancreas but was less obvious in treated groups. The mechanism of action of the UFD emerges to be due to increase the activity of antioxidant enzyme and secretion of pancreatic insulin.

          Conclusion

          Reduction in the FBG (fasting blood glucose), glycated hemoglobin, glucose-6-phosphatase, fructose-1-6-biphosphate, superoxide dismutase, catalase, glutathione peroxides, cholesterol, triglyceride, LDL, VLDL levels and improvement in the level of the plasma insulin, hexokinase, HDL was observed by the UFD treated rats. The result indicates that UFD has anti-diabetic activity along with anti hyperlipidemic and antioxidant efficacy and provides a scientific rationale to be used as an Anti-diabetic agent.

          Electronic supplementary material

          The online version of this article (doi:10.1186/2193-1801-2-639) contains supplementary material, which is available to authorized users.

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          Most cited references53

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          Selenium: biochemical role as a component of glutathione peroxidase.

          When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.
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            A simplified method of evaluating dose-effect experiments.

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              Postprandial hyperglycemia and diabetes complications: is it time to treat?

              A Ceriello (2004)
              Increasing evidence suggests that the postprandial state is a contributing factor to the development of atherosclerosis. In diabetes, the postprandial phase is characterized by a rapid and large increase in blood glucose levels, and the possibility that the postprandial "hyperglycemic spikes" may be relevant to the onset of cardiovascular complications has recently received much attention. Epidemiological studies and preliminary intervention studies have shown that postprandial hyperglycemia is a direct and independent risk factor for cardiovascular disease (CVD). Most of the cardiovascular risk factors are modified in the postprandial phase in diabetic subjects and directly affected by an acute increase of glycemia. The mechanisms through which acute hyperglycemia exerts its effects may be identified in the production of free radicals. This alarmingly suggestive body of evidence for a harmful effect of postprandial hyperglycemia on diabetes complications has been sufficient to influence guidelines from key professional scientific societies. Correcting the postprandial hyperglycemia may form part of the strategy for the prevention and management of CVDs in diabetes.
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                Author and article information

                Contributors
                phvikas@gmail.com
                danishjhamdard@gmail.com
                firoz_anwar2000@yahoo.com
                phytomali@gmail.com
                mohdmujeeb72@gmail.com
                Journal
                Springerplus
                Springerplus
                SpringerPlus
                Springer International Publishing (Cham )
                2193-1801
                28 November 2013
                28 November 2013
                2013
                : 2
                : 639
                Affiliations
                [ ]Department of Pharmaceutical Sciences, Faculty of Health Sciences, Sam Higginbottom Institute of Agriculture, Technology & Sciences, Allahabad, Uttar Pradesh 211007 India
                [ ]Sidharatha Institute of Pharmacy, Dehradun, Uttrakhand 248001 India
                [ ]Department of Phytochemisty & Pharmacognosy, Faculty of Pharmacy, Jamia Hamdard, New Delhi 110062 India
                Article
                693
                10.1186/2193-1801-2-639
                3862866
                24349947
                06aa50a5-3f73-488b-b51c-948176dec31c
                © Kumar et al.; licensee Springer. 2013

                This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 September 2013
                : 13 November 2013
                Categories
                Research
                Custom metadata
                © The Author(s) 2013

                Uncategorized
                streptozotocin,antihyperlipidemic,glibenclamide,umbelliferon-α-d-glucopyranosyl-(2i → 1ii)-α-d-glucopyranoside,antidiabetic

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