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. 2011 Jun 29;8(1):46.
doi: 10.1186/1743-7075-8-46.

Cinnamon Extract Inhibits α-Glucosidase Activity and Dampens Postprandial Glucose Excursion in Diabetic Rats

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Cinnamon Extract Inhibits α-Glucosidase Activity and Dampens Postprandial Glucose Excursion in Diabetic Rats

H Mohamed Sham Shihabudeen et al. Nutr Metab (Lond). .
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Abstract

Background: α-glucosidase inhibitors regulate postprandial hyperglycemia (PPHG) by impeding the rate of carbohydrate digestion in the small intestine and thereby hampering the diet associated acute glucose excursion. PPHG is a major risk factor for diabetic vascular complications leading to disabilities and mortality in diabetics. Cinnamomum zeylanicum, a spice, has been used in traditional medicine for treating diabetes. In this study we have evaluated the α-glucosidase inhibitory potential of cinnamon extract to control postprandial blood glucose level in maltose, sucrose loaded STZ induced diabetic rats.

Methods: The methanol extract of cinnamon bark was prepared by Soxhlet extraction. Phytochemical analysis was performed to find the major class of compounds present in the extract. The inhibitory effect of cinnamon extract on yeast α-glucosidase and rat-intestinal α-glucosidase was determined in vitro and the kinetics of enzyme inhibition was studied. Dialysis experiment was performed to find the nature of the inhibition. Normal male Albino wistar rats and STZ induced diabetic rats were treated with cinnamon extract to find the effect of cinnamon on postprandial hyperglycemia after carbohydrate loading.

Results: Phytochemical analysis of the methanol extract displayed the presence of tannins, flavonoids, glycosides, terpenoids, coumarins and anthraquinones. In vitro studies had indicated dose-dependent inhibitory activity of cinnamon extract against yeast α-glucosidase with the IC 50 value of 5.83 μg/ml and mammalian α-glucosidase with IC 50 value of 670 μg/ml. Enzyme kinetics data fit to LB plot pointed out competitive mode of inhibition and the membrane dialysis experiment revealed reversible nature of inhibition. In vivo animal experiments are indicative of ameliorated postprandial hyperglycemia as the oral intake of the cinnamon extract (300 mg/kg body wt.) significantly dampened the postprandial hyperglycemia by 78.2% and 52.0% in maltose and sucrose loaded STZ induced diabetic rats respectively, compared to the control. On the other hand, in rats that received glucose and cinnamon extract, postprandial hyperglycemia was not effectively suppressed, which indicates that the observed postprandial glycemic amelioration is majorly due to α-glucosidase inhibition.

Conclusions: The current study demonstrates one of the mechanisms in which cinnamon bark extract effectively inhibits α-glucosidase leading to suppression of postprandial hyperglycemia in STZ induced diabetic rats loaded with maltose, sucrose. This bark extract shows competitive, reversible inhibition on α-glucosidase enzyme. Cinnamon extract could be used as a potential nutraceutical agent for treating postprandial hyperglycemia. In future, specific inhibitor has to be isolated from the crude extract, characterized and therapeutically exploited.

Figures

Figure 1
Figure 1
Inhibition of yeast α-glucosidase by CZ extract. A. Inhibition of α-glucosidase by CZ extract at various concentrations (1-16 μg/ml). B. Inhibition α-glucosidase by acarbose at various concentrations (1-60 μg/ml). The α-glucosidase inhibition was analyzed by measuring p-nitrophenol released from PNPG at 405 nm after 30 minutes of incubation at 37°C. Results are expressed as mean of percent inhibition ± S.E.M against log 10 concentration of inhibitor.
Figure 2
Figure 2
Inhibition of Mammalian α-glucosidase by CZ extract. A. Inhibition of mammalian α-glucosidase by CZ extract at various concentrations (0.3-2.1 mg/ml). B. Inhibition mammalian α-glucosidase by acarbose at various concentrations (20-140 μg/ml). The α-glucosidase inhibition was analyzed by measuring p-nitrophenol released from pNPG at 405 nm after 30 minutes of incubation at 37°C. Results are expressed as mean of percent inhibition ± S.E.M against log 10 concentration of inhibitor.
Figure 3
Figure 3
Mode of α-glucosidase inhibition by CZ extract. Lineweaver-Burk plot of α- glucosidase inhibition by CZ. α-glucosidase was treated with various concentrations of pNP-glycoside (0.5-4 mM) in the absence or presence of CZ at two different concentrations (0.5 and 1 mg/ml). The kinetics assay has been performed after incubating the mixture at 37°C for 30 min.
Figure 4
Figure 4
Reversibility of CZ action. α-glucosidase (100 U) was incubated with CZ (23.5 mg) in 0.5 ml of sodium phosphate buffer (50 mM; pH 6.7) for 2 h at 37°C and dialyzed against sodium phosphate buffer (5 mM; pH 6.7) at 4°C for 24 h. Reversibility of CZ was determined by comparing the residual enzyme activity after dialysis with that of non-dialyzed one. α-glucosidase alone (EC, ED) and the complex of α-glucosidase and CZ (EIC, EID) were dialyzed against 5 mM sodium phosphate buffer (pH 6.7) at 4°C (ED, EID) or were kept at 4°C (EC, EIC) for 24 h.
Figure 5
Figure 5
Inhibitory effects of CZ on blood glucose after maltose loading in normal rats. The normal rats fasted for 16 h received maltose (2 g/kg body wt; p.o.) and dose of CZ (300 mg/kg body wt; p.o.) by gastric intubation. Control group received maltose (2 g/kg body wt; p.o.) alone, and the drug control group received maltose (2 g/kg body wt; p.o.) plus acarbose (5 mg/kg). Blood glucose was measured at 0, 30, 60 and 120 min after food administration. A. The glycemic response curve in normal rats after maltose challenge. B. The incremental AUC0-120 min in normal rats after maltose administration. Data are expressed as the mean ± S.E, n = 6. *, P < 0.05 vs. control; **, P < 0.01 vs. control; ***, P < 0.001 vs. control.
Figure 6
Figure 6
Inhibitory effect of CZ on blood glucose after maltose loading in diabetic rats. The diabetic rats fasted for 16 h received maltose (2 g/kg body wt; p.o.) and different doses of CZ (300 mg/kg body wt; p.o. and 600 mg/kg body wt; p.o.) by gastric intubations. Control animals were given only maltose (2 g/kg body wt; p.o.) and the drug control group received maltose (2 g/kg body wt; p.o.) plus acarbose (5 mg/kg). Blood glucose was monitored at 0, 30, 60 and 120 min after food administration. The result shows the significantly impeded 30 minutes post-load glucose level in the CZ 300 mg and CZ 600 mg treated group compared to control. Data are expressed as the mean ± S.E, n = 6. *, P < 0.05 vs. control; **, P < 0.01 vs. control; ***, P < 0.001 vs. control.
Figure 7
Figure 7
Inhibitory effects of CZ on blood glucose after sucrose loading in normal rats. The normal rats fasted for 16 h received sucrose (2 g/kg body wt; p.o.) and dose of CZ (300 mg/kg body wt; p.o.) by gastric intubation. Control group received sucrose (2 g/kg body wt; p.o.) alone and the drug control group received sucrose (2 g/kg body wt; p.o.) plus acarbose (5 mg/kg). Blood glucose was measured at 0, 30, 60 and 120 min after food administration. A. The glycemic response curve in normal rats after sucrose challenge. B. The incremental AUC0-120 min in normal rats after sucrose administration. Data are expressed as the mean ± S.E, n = 6. *, P < 0.05 vs. control; **, P < 0.01 vs. control; ***, P < 0.001 vs. control.
Figure 8
Figure 8
Inhibitory effect of CZ on blood glucose after sucrose loading in diabetic rats. The diabetic rats fasted for 16 h received sucrose (2 g/kg body wt; p.o.) and a dose of CZ (300 mg/kg body wt; p.o.) by gastric intubations. Control animals were given only sucrose (2 g/kg body wt; p.o.) and the drug control group received sucrose (2 g/kg body wt; p.o.) plus acarbose (5 mg/kg). Blood glucose was monitored at 0, 30, 60 and 120 min after food administration. A. The glycemic response curve in diabetic rats after sucrose challenge. B. The incremental AUC0-120 min in diabetic rats after sucrose administration. Data are expressed as the mean ± S.E, n = 6. *, P < 0.05 vs. control; **, P < 0.01 vs. control; ***, P < 0.001 vs. control.
Figure 9
Figure 9
Inhibitory effect of CZ on blood glucose after glucose loading in normal rats. The rats fasted for 16 h received glucose (2 g/kg body wt; p.o.) and a dose of CZ (300 mg/kg body wt; p.o.) by gastric intubations. Control animals were given only glucose (2 g/kg body wt; p.o.). Blood glucose was monitored at 0, 30, 60 and 120 min after food administration. There are no significant changes observed in the 30 minutes post-load glucose level between the control group and CZ treated group. Data are expressed as the mean ± S.E, n = 6. ns- not significant.
Figure 10
Figure 10
Inhibitory effect of CZ on blood glucose after glucose loading in diabetic rats. The diabetic rats fasted for 16 h received glucose (2 g/kg body wt; p.o.) and a dose of CZ (300 mg/kg body wt; p.o.) by gastric intubations. Control animals were given only glucose (2 g/kg body wt; p.o.). Blood glucose was monitored at 0, 30, 60 and 120 min after food administration. There are no significant changes observed in the 30 minutes post-load glucose level between the control group and CZ treated group. Data are expressed as the mean ± S.E, n = 6. ns- not significant.

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