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Antihyperglycemic and antinociceptive effects of a commercially produced beta-glucan from Saccharomyces cerevisiae in Swiss albino mice.

Introduction

Beta-glucans are sugars that are found in the cell walls of bacteria, fungi, yeasts, algae, lichens, and plants, such as oats and barley. They are polysaccharides of D-glucose monomers linked by beta-glycosidic bonds. Their major use is as a nutraceutical and it has been claimed that these compounds can act as effective immune modulators through boosting the immune system. The most active forms of beta- glucans are those comprising D-glucose units with (1,3) links and with side-chains of D-glucose attached at the (1,6) position.

Beta-glucans, differing in molecular weight, have been isolated from many diverse species like Rhynchelytrum repens, Lentinus edodes, Grifola frondosa, Tremella mesenterica, Tremella aurantia, Zea mays, Agaricus blazei (mushroom), Phellinus buammi, and Saccharomyces cerevisiae (yeast) (Rahar et al., 2011). The most common sources of beta-glucans have generally been maize, oats, and yeast. Beta-glucans, isolated from Agaricus blazei and their enzymatically hydrolyzed oligosaccharides derivatives have been shown to demonstrate anti-hyperglycemic, anti-hypertriglyceridemic, anti- hypercholesterolemic, and anti-arteriosclerotic activity in diabetic rats, indicating overall anti-diabetic activity (Kim et al., 2005). In human subjects, beta-glucan, isolated from oat bran, was found to lower peak values of glycemic responses than the reference glucose load (Makelainen et al., 2007). Aminated beta-1,3-D-glucan reportedly improved wound healing in diabetic db/db mice, suggesting a beneficial effect of beta-glucans in diabetes (Berdal et al., 2007). Indeed, dietary intake of beta-glucans has been shown to reduce risk factors arising from diabetes like high blood glucose level, manifestations of thirst, polyuria, polydipsia, and weight loss (Chen and Raymond, 2008).

Oat products, which are abundant in beta-glucan has been reported to lower the glycemic index of products or foods, which is beneficial in the control of postprandial glycemia. Streptozotocin-induced diabetic mice, fed oat products containing beta-glucan in their diet for 6 weeks, had significantly decreased fasting blood glucose and glycosylated serum protein (Shen et al., 2011). A synergistic favorable effect of bitter melon (Momordica charantia) and beta-glucan isolated from oats has been shown in streptozotocin- induced diabetic rats, when administered for 28 days (Kim et al., 2012). Hypoglycemic and hypocholesterolemic effects of botryosphaeran (a water-soluble exopolysaccharide of the beta-1[right arrow]3; 1[right arrow]6- D-glucan type) from Botryosphaeria rhodina has been observed following administration to diabetic rats over 15 days (Miranda- Nantes et al., 2011). Overall, the various reports suggest that beta-glucans isolated from various microbial and plant sources have an overall beneficial effect in diabetic rodent models, as well as in humans. These results point to an anti-diabetic effect of beta-glucans manifested primarily through reduction in blood sugar levels and lowering of glycemic index of foods. However, other complications arising from diabetes have also been reported to be reduced, especially following long-term administration of beta-glucans in diet or when administered alone through gavaging.

An anti-inflammatory and analgesic property of a (1[right arrow]3),(1[right arrow]6)-linked beta-glucan isolated from Pleurotus pulmonarius has also been shown in a rodent model (Smiderle et al., 2008). It is therefore evident that betaglucans from different sources possibly possess potential to be used as anti- hyperglycemic and analgesic agents on top of their being used as nutraceuticals, primarily to boost immune functions in the body. The objective of this study was to evaluate the anti-hyperglycemic and antinociceptive potential of a commercially available beta-glucan isolated from Saccharomyces cerevisiae.

Materials and Methods

Chemicals:

Glacial acetic acid was obtained from Sigma Chemicals, USA; aspirin, glibenclamide and glucose were obtained from Square Pharmaceuticals Ltd., Bangladesh. WGP[R] beta-glucan Wellmune was obtained from a nutraceutical shop at Kuala Lumpur, Malaysia. WGP is a registered trade mark of Biothera, Minnesota, USA. The product was manufactured by Pahang Pharmacy SDN.BHD, Selangor, Malaysia (Lot 5979, Batch Number 10N37, expiry date April 2013; this study was done in 2012). As per the information that came with the beta-glucan container, the beta-glucan was prepared from baker's yeast (Saccharomyces cerevisiae). The product was distributed as capsules, with each capsule containing 200 mg beta-glucan. The dosage for human consumption was mentioned in the information booklet to be one capsule per day on an empty stomach. Stock solution of beta-glucan was prepared in water (0.06g beta-glucan per ml distilled water).

Animals:

In the present study, Swiss albino mice (male), which weighed between 22-29g were used. The animals were obtained from International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B). All animals were kept under ambient temperature with 12h light followed by a 12h dark cycle. The animals were acclimatized for three days prior to actual experiments. The study was conducted following approval by the Institutional Animal Ethical Committee of University of Development Alternative, Dhaka, Bangladesh.

Antihyperglycemic activity:

Glucose tolerance property of the commercial beta-glucan was determined as per the procedure previously described by Joy and Kuttan (1999) with minor modifications. In brief, fasted mice were grouped into six groups of six mice each. The various groups received different treatments like Group 1 received vehicle (10 ml distilled water/kg body weight) and served as control, group 2 received standard drug (glibenclamide, 10 mg/kg body weight). Groups 3-6 received beta-glucan at doses of 30, 60, 120, and 240 mg per kg body weight. Each mouse was weighed and doses adjusted accordingly prior to administration of vehicle, standard drug, and test samples. All substances were orally administered. Following a period of one hour, all mice were orally administered 2 g glucose/kg of body weight. Blood samples were collected 120 minutes after the glucose administration through puncturing heart. Blood glucose levels were measured by glucose oxidase method (Venkatesh et al., 2004).

Antinociceptive activity:

Antinociceptive activity of beta-glucan was examined using previously described procedures (Shanmugasundaram and Venkataraman, 2005). Briefly, mice were divided into seven groups of six mice each. Group 1 served as control and was administered vehicle only. Groups 2 and 3 were orally administered the standard antinociceptive drug aspirin at a dose of 200 and 400 mg per kg body weight, respectively. Groups 4-7 were administered beta-glucan at doses of 30, 60, 120 and 240 mg per kg body weight, respectively. Following a period of 60 minutes after oral administration of standard drug or beta- glucan, all mice were intraperitoneally injected with 1% acetic acid at a dose of 10 ml per kg body weight. A period of 15 minutes was given to each animal to ensure bio-availability of acetic acid, following which period, the number of writhings was counted for 10 min.

Statistical analysis:

Experimental values are expressed as mean [+ or -] SEM. Independent Sample t- test was carried out for statistical comparison. Statistical significance was considered to be indicated by a p value < 0.05 in all cases.

Results and Discussion

The beta-glucan used in the present study showed significant and dose-dependent lowering of blood glucose levels in glucose-loaded mice at all the tested concentrations. At doses of 30, 60, 120 and 240 mg per kg body weight, the percent lowering in blood glucose levels were, respectively, 33.5, 35.0, 35.7 and 38.7. By comparison, a standard anti-hyperglycemic drug, glibenclamide, when administered at a dose of 10 mg per kg body weight reduced blood sugar in mice by 40.0%. Thus the beta-glucan, at least at the highest experimental dose tested, lowered blood glucose, which was comparable to that of glibenclamide. The results are shown in Table 1.

The blood glucose lowering capability exhibited by beta-glucan could be due to the reported ability of beta-glucan to lower the glycemic index of carbohydrates (Makelainen et al., 2007). The exact mechanism remains to be elucidated, but one possible factor behind the observed blood glucose lowering may be decreased absorption of glucose from the gut (Bhowmik et al., 2009). However, other mechanism(s) cannot be ruled out, like potentiating insulin secretion from the pancreas (Farjou et al., 1987). It is to be noted that at least one published study has found evidences to that effect in case of beta-glucan (Makelainen et al., 2007).

In antinociceptive activity tests, beta-glucan at doses of 30, 60, 120 and 240 mg per kg body weight inhibited the number of writhings in mice induced by intraperitoneal administration of acetic acid, respectively, by 36.6, 40.0, 43.4 and 60.0%. The percent reductions in the number of writhings were both significant as well as dose-dependent. The results are shown in Table 2. The standard antinociceptive drug, aspirin, when administered at doses of 200 and 400 mg per kg body weight, reduced the number of writhings by 40.0 and 63.4%, respectively. Thus, beta-glucan showed considerable antinociceptive activity, which was directly comparable to that of aspirin.

Anti-inflammatory and analgesic property of a (1[right arrow]3),(1[right arrow]6)-linked beta-glucan isolated from Pleurotus pulmonarius has also been shown in a rodent model (Smiderle et al., 2008). In this case, the beta-glucan was from Saccharomyces cerevisiae. We have not elucidated the exact mechanism behind the antinociceptive activity of the beta-glucan, but it may be hypothesized that this activity has to do with possible inhibition of cyclooxygenases, which synthesize prostaglandins [mainly prostacyclines (PGI2) and prostaglandin-(PG-E)], which has been shown to be responsible for excitation of Adelta-nerve fibers, leading to the sensation of pain (Reynolds, 1982; Rang and Dale, 2003).

Overall, the results obtained from the commercially produced beta-glucan isolated from Saccharomyces cerevisiae suggest that besides its intended use as a nutraceutical (with possible immunomodulatory benefits), the product may also be used by diabetic patients for lowering blood sugar and by people affected with pain. The results further suggest that more studies should be carried out with beta- glucans from different sources [particularly the (1[right arrow]3),(1[right arrow]6) type] to fully determine the pharmacological and beneficial effects of these type of glucans.

Funding:

Authors of this study have no financial interest in any of the product(s) or manufacturer(s) mentioned in this article.

References

Berdal, M., H.I. Appelbom, J.H. Eikrem, A. Lund, S. Zykova, L.T. Busund, R. Seljelid and T. Jenssen, 2007. Animated beta-1,3-D-glucan improves wound healing in diabetic db/db mice. Wound Repair and Regeneration, 15: 825-832.

Bhowmik, A., L.A. Khan, M. Akhter and B. Rokeya, 2009. Studies on the antidiabetic effects of Mangifera indica stem-barks and leaves on nondiabetic, type 1 and type 2 diabetic model rats. Bangladesh Journal of Pharmacology, 4: 110-114.

Chen, J. and K. Raymond, 2008. Beta-glucans in the treatment of diabetes and associated cardiovascular risks. Vascular Health and Risk Management, 4: 1265-1272.

Farjou, I.B., M. Al-Ani and S.Y. Guirgea, 1987. Lowering of blood glucose of diabetic rats by Artemisia extract. Journal of the Faculty of Medicine, 92: 137-147.

Joy, K.L. and R.J. Kuttan, 1999. Anti-diabetic activity of Picrorrhiza kurroa extract. Journal of Ethnopharmacology, 67: 143-148.

Kim, J.W., H.R. Cho, S.B. Moon, K.Y. Kim and S. Ku, 2012. Synergic effects of bitter melon and beta-glucan composition on STZ-induced rat diabetes and its complications. Journal of Microbiology and Biotechnology, 22: 147-155.

Kim, Y.W., K.H. Kim, H.J. Choi and D.S. Lee, 2005. Anti-diabetic activity of beta-glucans and their enzymatically hydrolyzed oligosaccharides from Agaricus blazei. Biotechnology Letters, 27: 483-487.

Makelainen, H., H. Anttila, J. Sihvonen, R.M. Hietanen, R. Tahvonen, E. Salminen, M. Mikola and T. Sontag-Strohm, 2007. The effect of beta-glucan on the glycemic and insulin index. European Journal of Clinical Nutrition, 61: 779-785.

Miranda-Nantes, C.C., E.A. Fonseca, C.T. Zaia, R.F. Dekker, N. Khaper, I.A. Castro and A.M. Barbosa, 2011. Hypoglycemic and hypocholesterolemic effects of botryosphaeran from Botryosphaeria rhodina MAMB05 in diabetes-induced and hyperlipidemia conditions in rats. Mycobiology, 39: 187- 193.

Rahar, S., G. Swami, N. Nagpal, M.A. Nagpal and G.S. Singh, 2011. Preparation, characterization, and biological properties of beta-glucans. Journal of Advanced Pharmaceutical Technology & Research, 2: 94-103.

Rang, H.P., M.M. Dale, J.M. Ritter and P.K. Moore, 2003. Pharmacology, Churchill Livingstone, 5th Edition; pp: 562-563.

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Shanmugasundaram, P. and S. Venkataraman, 2005. Anti-nociceptive activity of Hygrophilous auriculata (Schum) Heine. African Journal of Traditional, Complementary and Alternative Medicines, 2: 62-69.

Shen, R.L., F.L. Cai, J.L. Dong and X.Z. Hu, 2011. Hypoglycemic effects and biochemical mechanisms of oat products on streptozotocin-induced diabetic mice. Journal of Agricultural and Food Chemistry, 59: 8895-8900.

Smiderle, F.R., L.M. Olsen, E.R. Carbonero, C.H. Baggio, C.S. Freitas, R. Marcon, A.R. Santos, P.A. Gorin and M. Iacomini, 2008. Anti-inflammatory and analgesic properties in a rodent model of a (1[right arrow]3),(1[right arrow]6)-linked beta-glucan isolated from Pleurotuspulmonarius. European Journal of Pharmacology, 597: 86-91.

Venkatesh, S., G.D. Reddy, Y.S.R. Reddy, D. Sathyavathy and B.M. Reddy, 2004. Effect of Helicteres isora root extracts on glucose tolerance in glucose-induced hyperglycemic rats. Fitoterapia, 75: 364-367.

(1) Md. Tanvir Morshed, (1) Shahnaz Rahman, (1) Shiblur Rahman, (1) Sharmin Jahan, (2) Mohsina Mukti, (2) Inin Taznin, (1) Masta Hasenur Reza Chawdhury, (1) Mohammed Rahmatullah

(1) Faculty of Life Sciences, University of Development Alternative, Dhaka-1209, Bangladesh.

(2) Department of Pharmacy, North South University, Bashundhara, Dhaka-1229, Bangladesh.

Md. Tanvir Morshed, Shahnaz Rahman, Shiblur Rahman, Sharmin Jahan, Mohsina Mukti, Inin Taznin, Masta Hasenur Reza Chawdhury, Mohammed Rahmatullah; Antihyperglycemic and antinociceptive effects of a commercially produced beta-glucan from Saccharomyces cerevisiae in Swiss albino mice

Corresponding Author: _Professor Dr. Mohammed Rahmatullah, Pro-Vice Chancellor and Dean, Faculty of Life Sciences, University of Development Alternative, House No. 78, Road No. 11A (new), Dhanmondi, Dhaka-1205, Bangladesh

Telephone: +88-01715032621 Fax: +88-02-815739 Email: rahamatm@hotmail.com
Table 1: Effect of beta-glucan on blood glucose level in
hyperglycemic mice following 120 minutes of glucose loading.

Treatment                  Dose (mg/kg        Blood glucose
                           body weight)       level (mmol/l)

Control (Group 1)              10 ml        6.80 [+ or -] 0.24
Glibenclamide (Group 2)        10 mg       4.08 [+ or -] 0.0.42
Beta-glucan (Group 3)          30 mg        4.52 [+ or -] 0.42
Beta-glucan (Group 4)          60 mg        4.42 [+ or -] 0.25
Beta-glucan (Group 5)         120 mg        4.37 [+ or -] 0.39
Beta-glucan (Group 6)         240 mg        4.17 [+ or -] 0.30

Treatment                   % lowering
                              of blood
                           glucose level

Control (Group 1)                --
Glibenclamide (Group 2)        40.0 *
Beta-glucan (Group 3)          33.5 *
Beta-glucan (Group 4)          35.0 *
Beta-glucan (Group 5)          35.7 *
Beta-glucan (Group 6)          38.7 *

All administrations were made orally. Values represented as mean [+
or -] SEM, (n=6); * P < 0.05; significant compared to hyperglycemic
control animals.

Table 2: Antinociceptive effect of beta-glucan in the acetic acid-
induced gastric pain model mice.

Treatment                Dose (mg/kg        Mean number
                         body weight)       of writhings

Control (Group 1)            10 ml       5.00 [+ or -] 0.52
Aspirin (Group 2)           200 mg       3.00 [+ or -] 0.73
Aspirin (Group 3)           400 mg       1.83 [+ or -] 0.83
Beta-glucan (Group 4)        30 mg       3.17 [+ or -] 0.48
Beta-glucan (Group 5)        60 mg       3.00 [+ or -] 0.52
Beta-glucan (Group 6)       120 mg       2.83 [+ or -] 0.48
Beta-glucan (Group 7)       240 mg       2.00 [+ or -] 0.45

Treatment                     %
                          inhibition

Control (Group 1)             --
Aspirin (Group 2)           40.0 *
Aspirin (Group 3)           63.4 *
Beta-glucan (Group 4)       36.6 *
Beta-glucan (Group 5)       40.0 *
Beta-glucan (Group 6)       43.4 *
Beta-glucan (Group 7)       60.0 *

All administrations (aspirin and beta-glucan) were made orally.
Values represented as mean [+ or -] SEM, (n=6); * P < 0.05;
significant compared to control.
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Title Annotation:Original Article
Author:Morshed, Tanvir; Rahman, Shahnaz; Rahman, Shiblur; Jahan, Sharmin; Mukti, Mohsina; Taznin, Inin; Cha
Publication:Advances in Natural and Applied Sciences
Article Type:Report
Date:Jul 1, 2013
Words:2562
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