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British Journal of Pharmacology and Toxicology 3(6): 278-288, 2012 ISSN: 2044-2459; E-ISSN: 2044-2467 Maxwell Scientific Organization, 2012 Submitted: September 11, 2012 Accepted: October 09, 2012 Comparative Effects of Glimepiride, Vanadyl Sulfate and Their Combination on
Hypoglycemic Parameters and Oxidative Stress
1Marwa M.A. Khalaf, 1Gamal A. El Sherbiny, 2Hekma A. AbdEllatif, 2Afaf A. Ain-shoka, 2Mostafa E. El Sayed 1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, 62511, Egypt 2Departments of Pharmacology and Toxicology, Faculty of Pharmacy, Abstract: The present study was performed to evaluate the effect of glimepiride, Vanadyl Sulfate (VOSO4) or their
combination on glycemic status and oxidative stress in STZ-diabetic rats and to investigate the possible mechanism
of action of these drugs. Another aim of this study is to determine whether there is a possible interaction between
certain chosen trace element (VOSO4) and glimepiride as representative to oral hypoglycemic agents. Treatment of
STZ-diabetic animals with glimepiride (10 mg/kg, p.o.) or VOSO4 (15 mg/kg, i.p.) decreased serum glucose level
and increased liver glycogen content. Glimepiride increased serum insulin level and glucose (6 mmol/L)-stimulated
insulin secretion from isolated rat pancreatic islets. Vanadyl sulfate did not affect serum insulin level or glucose (6
mmol/L)-stimulated insulin secretion from isolated rat pancreatic islets. Glimepiride and VOSO4 increased plasma
GSH level, plasma SOD level and decreased serum TBARS level. Combination of VOSO4 with glimepiride did not
improve the effect of glimepiride alone on any of the measured parameters when given in the selected doses
indicating no significant interaction between these two drugs on the selected parameters. It could be concluded that
concurrent administration of VOSO4 with glimepiride does not produce any additive effect on any of the measured
parameters. Therefore, VOSO4 can be taken safely as a micronutrient in diabetic patient treated with glimepiride
without fear of any serious reactions.
Keywords: Diabetes, glimepiride, hypoglycemic parameters, oxidative stress, vanadyl sulfate
INTRODUCTION
oral hypoglycemic agent of the sulfonylurea group (See et al., 2003). However, glimepiride suffers from severe Type 2 Diabetes Mellitus (T2DM) is a chronic side effects such as gastrointestinal disorders (Paice metabolic disorder characterized mainly by et al., 1985), hypersensitivity reactions (Paice et al., hyperglycemia (Barnett, 2009) which results from 1985) and severe hypoglycemia which may be life- either a decrease in insulin secretion or from insulin resistance in the target tissues (Tian et al., 2006). Therefore, there is a need to search for newer and Diabetes Mellitus is the major cause of many alternative therapy for T2DM to be more effective and serious complications such as cardiovascular disorders (Ewais et al., 2005), diabetic foot (Demiot et al., 2006), Vanadium is a trace element present in low concentration in animals (Zorzano et al., 2009) and mammals (Bolkent et al., 2005), which has been nephropathy (Yin et al., 2004), retinopathy (Santoso, previously reported to exert antidiabetic action (Cohen 2006) and depression leading to mortality (Antai- et al., 1995; Goldfine et al., 1995; Boden et al., 1996; Otong, 2007; De Groot et al., 2007). In addition, oxidative stress has been reported to Consequently, it deemed necessary in the present play an important role in T2DM (Siddiqui et al., 2005; study to examine the possible antidiabetic and antioxidant effects of vanadyl sulfate as well as Administration of oral hypoglycemic agents is glimepiride alone and in combination. The study of co- necessary for achievement of the required glycemic administration of vanadyl sulfate with glimepiride control (DeFronzo, 1999). Glimepiride is an important Corresponding Author: Marwa M.A. Khalaf, Department of pharmacology and toxicology, faculty of pharmacy, Beni-Suef
University, Beni-Suif, 62511, Egypt, Tel.: 01002784548, Fax: 0822317958 Br. J. Pharmacol. Toxicol., 3(6): 278-288, 2012 MATERIAL AND METHODS
Experimental design:
In vivo experiment: Rats were divided into 5 groups,
Animals: Adult Sprague Dawley male rats weighing
each consisting of 6-8 rats. Four groups of them were 150±20 g for in vivo experiments and 200±20 g for in made diabetic by STZ (50 mg/kg i.p.), the remaining vitro experiment were used in this study. Animals were group was considered as normal control and received an obtained from National Research Center, Cairo, Egypt. equivalent volume of citrate buffer. These diabetic rats Rats were housed in plastic cages and were maintained were randomly classified into 4 groups; one of them under conventional laboratory conditions throughout received 1% Tween 80 and was considered as diabetic the study. They were fed standard pellet chow (El-Nasr control. The remaining 3 groups received glimepiride (10 mg/kg p.o.), vanadyl sulfate (15 mg/kg i.p.) or chemical Co., Abu Zaabal, Cairo and Egypt.) and combination of both glimepiride and vanadyl sulfate, allowed water ad libitum. All procedures in this study respectively. These treatments were started 72 h after were carried out according to guidelines of Ethics In vitro experiment: Isolated rat pancreatic islets were
divided into 4 groups. Each group consists of 5-6 Drugs and chemicals: STZ was purchased from
Wassermann tubes, each containing batch of 5 islets Sigma-Aldrich Chemical Co. (U.S.A.). Glimepiride was and incubated with 1 mL KRH buffer supplemented provided as a gift from SEDICO Company, Egypt. It with 0.5% bovine serum albumin and glucose 6 was suspended in 2% Tween 80 and orally administered mmol/L, one of these groups was considered as normal in a dose of 10 mg /kg (Ladriere et al., 1997). For in control. In the remaining 3 groups, the following drugs vitro experiments a dose of 10 µmol/L was chosen were added: glimepiride (10 µmol/L), vanadyl sulfate according to (Hu et al., 2001). Vanadyl sulfate was (1 µmol/L) or combination of both glimepiride and purchased from Sigma-Aldrich Chemical Co. (U.S.A.). vanadyl sulfate, respectively. All the tubes were It was freshly prepared by dissolving the powder in covered and incubated at 37°C in a shaking water bath saline to be given intraperitoneally in a dose of 15 for 1 h, then the tubes were transferred into ice-bath, mg/kg (Cadene et al., 1996). For in vitro experiments mixed with vortex mixer and aliquots of 0.5 mL were a dose of 1 µmol/L was chosen according to (Cadene taken and kept frozen at -20°C for insulin
Biochemical estimations:
Induction of experimental diabetes: Experimental
In vivo experiments: Serum glucose level was
diabetes was induced in 18 h fasted rats by single i.p. estimated using glucose kit (spinreact, Spain) (Trinder, injection of Streptozotocin (STZ) in a dose of 50 mg/kg 1969) and expressed as mg/dL. Whereas, serum insulin (Hounsom et al., 1998) freshly prepared in cold 0.1 M was assayed using radioimmunoassay kits (Coat-a- citrate buffer (pH 4.5). STZ-injected rats were provided Count kit -DPC, Los Angeles, CA, USA) (Mullner with a 5% glucose drinking solution for the first 24 h to et al., 1991) and expressed as µIU/mL. ensure survival (Hajduch et al., 1998). Normal control Liver glycogen was estimated (Kemp and Van group was injected with citrate buffer alone. Animals Heijningen, 1954) and expressed as mg/g wet tissue. were considered diabetic when their blood glucose level Serum lipid peroxides level was estimated by exceeded 250 mg/dL (Cam et al., 2003) and were determination of the level of Thiobarbituric Acid included in the study after 72 h of STZ injection. Reactive Substances (TBARS) that were measured as MDA (Mihara and Uchiyama, 1978) and expressed as Isolation and incubation of rat pancreatic islets:
Pancreatic islets were isolated following collagens Blood SOD was estimated using the pyrogallol digestion technique according to the method of (Lacy method (Marklund and Marklund, 1974) and expressed and Kostianovsky, 1967). The islets were pre-incubated into Wassermann tube containing fresh Krebs-Ringer- Blood GSH was estimated according to the method HEPES (KRH) solution and incubated at 37°C for 30 of (Beutler et al., 1963) and expressed as mg %. min in a shaking water bath for adaptation (LACY et al., 1968). Finally, Batches of 5 islets were picked up In vitro experiment: Insulin level was measured using
and incubated in small tubes, each containing 1 mL radioimmunoassay kits (Coat-a-Count kit -DPC, Los KRH buffer supplemented with 0.5% bovine serum Angeles, CA, USA) (Mullner et al., 1991) and albumin, glucose 6 mmol/L and the test drug. Br. J. Pharmacol. Toxicol., 3(6): 278-288, 2012 Statistical analysis: The values of the measured
the effect of glimepiride alone on serum insulin level in parameters were presented as mean±S.E.M. Comparisons between different treatments were carried out using one way Analysis of Variance (ANOVA) Effect of glimepiride, vanadyl sulfate or their
followed by Tukey-Kramer as post ANOVA multiple combination on liver glycogen content in STZ-
comparisons test. Differences were considered induced diabetic rats after two weeks of daily dose
statistically significant when p<0.05.
administration: STZ significantly reduced liver
glycogen content in diabetic control group. Glimepiride and vanadyl sulfate significantly increased liver glycogen content of diabetic rats to 195.26 and Effect of glimepiride, vanadyl sulfate or their
177.299% of the diabetic control value, respectively. combination on serum glucose and insulin levels in
Combination of vanadyl sulfate and glimepiride, when STZ-induced diabetic rats after two weeks of daily
given in the selected doses, did not significantly change dose administration: STZ significantly increased
the effect of glimepiride on liver glycogen content serum glucose level and significantly reduced the serum Glimepiride and vanadyl sulfate significantly reduced the serum glucose level to 54.77 and 57.35% of Effect of glimepiride, vanadyl sulfate or their
the diabetic control value, respectively. Combination of combination on oxidative stress biomarkers in STZ-
vanadyl sulfate and glimepiride did not significantly induced diabetic rats after 2 weeks of daily dose
affect the hypoglycemic action of glimepiride (Fig. 1). administration: STZ significantly lowered the blood
Glimepiride significantly increased the serum GSH level in diabetic rats. Glimepiride normalized the insulin level to 220.46 % of the diabetic control value. blood GSH level of diabetic rats to 81.49% of the However, vanadyl sulfate was unable to normalize the normal control value. However, this value was still non- decreased serum insulin level induced by STZ. significant from that of the diabetic control group Concurrent administration of vanadyl sulfate and recording 150.05% of the diabetic control value. glimepiride, in the selected doses, could not improve Vanadyl sulfate significantly elevated the blood Fig. 1: Effect of glimepiride, vanadyl sulfate or their combination on serum glucose level in STZ-induced diabetic rats after two weeks of daily dose administration Diabetes was induced by a single injection of STZ (50 mg/kg, i.p.) in all groups except the normal control one, which received an equivalent volume of citrate buffer. Drug treatment was started 72 h after STZ administration once daily, for two successive weeks. Blood samples were collected 2 h after the last dose administration; N: 6-7 rats per group; Data were expressed as mean±S.E. of the mean; *: Significantly different from the normal control value at p<0.05; a: Significantly different from diabetic control value at p<0.05 Br. J. Pharmacol. Toxicol., 3(6): 278-288, 2012 Fig. 2: Effect of glimepiride, vanadyl sulfate or their combination on serum insulin level in STZ-induced diabetic rats after 2 weeks of daily dose administration Diabetes was induced by a single injection of STZ (50 mg/kg, i.p.) in all groups except the normal control one, which received an equivalent volume of citrate buffer. Drug treatment was started 72 h after STZ administration once daily, for two successive weeks. Blood samples were collected 2 h after the last dose administration; N: 6-7 rats per group; Data were expressed as mean±S.E. of the mean; *: Significantly different from the normal control value at p<0.05; a: significantly different from diabetic control value at p<0.05; b: Significantly different from glimepiride value at p<0.05 Fig. 3: Effect of glimepiride, vanadyl sulfate or their combination on liver glycogen content in STZ-induced diabetic rats after two weeks of daily dose administration Diabetes was induced by a single injection of STZ (50 mg/kg, i.p.) in all groups except the normal control one, which received an equivalent volume of citrate buffer. Drug treatment was started 72 h after STZ administration once daily, for two successive weeks. Liver was isolated 2 h after the last dose administration and homogenized in saline to be used for determination of glycogen content; N: 6-7 rats per group; Data were expressed as mean±S.E. of the mean; *: Significantly different from the normal control value at p<0.05; a: Significantly different from diabetic control value at p<0.05 Br. J. Pharmacol. Toxicol., 3(6): 278-288, 2012 Fig. 4: Effect of glimepiride, vanadyl sulfate or their combination on (6 mmol/L) glucose-stimulated insulin secretion from isolated rat pancreatic islets Islets were isolated from non-fasting rats according to the collagenase digestion technique and pre-incubated in Krebs-Ringer-HEPES medium (KRH) at 37ºC for 30 min. After the pre-incubation period, batches of five islets were transferred to a medium containing 1 mL KRH buffer supplemented with 0.5% bovine serum albumin, glucose (6 mmol/L), and the specified drug. Islets were incubated at 37ºC in a shaking water bath for 1 h. After the incubation period, the medium was assayed for insulin content; N: 5-6 rats per group; Data were expressed as mean±S.E. of the mean; *: Significantly different from the control value at p<0.05; a: Significantly different from glimepiride value at p<0.05 Table 1: Effect of glimepiride, vanadyl sulfate or their combination on oxidative stress biomarkers in STZ-induced diabetic rats after 2 weeks of --------------------------------------------------------------------------------------------------------------------- (citrate buffer and Tween 80) Diabetic control (10 mg/kg, p.o.) Vanadyl sulfate (VOSO4) (10 mg/kg,p.o.) + (15 mg/kg, i.p.) Diabetes was induced by a single injection of STZ (50 mg/kg, i.p.) in all groups except the normal control one, which received an equivalent volume of citrate buffer. Drug treatment was started 72 h after STZ administration once daily, for two successive weeks. Blood samples were collected 2 h after the last dose administration; N: 6-7 rats per group; Data were expressed as mean±S.E. of the mean; *: Significantly different from the normal control value at p<0.05; a: Significantly different from diabetic control value at p<0.05 GSH level to 149.09% of the diabetic control value. It glimepiride alone on serum TBARS level indicating is evident that there was no significant interaction there is no significant interaction between these two between vanadyl sulfate and glimepiride when given in STZ caused a significant reduction in superoxide STZ induced a significant increase in serum dismutase level in the diabetic control rats. Glimepiride TBARS level in diabetic control rats. Glimepiride and and vanadyl sulfate significantly increased superoxide vanadyl sulfate significantly lowered serum TBARS dismutase value to 167.64 and 167.64% of the diabetic level of diabetic rats to 49.35 and 53.896% as compared control value, respectively. Combination of vanadyl to diabetic control value, respectively. Combination of sulfate and glimepiride was not significantly different vanadyl sulfate and glimepiride had the same effect of when compared to glimepiride monotherapy (Table 1). Br. J. Pharmacol. Toxicol., 3(6): 278-288, 2012 Effect of glimepiride, vanadyl sulfate or their
plasma insulin level, indicating that glimepiride has, in combination on (6 mmol/L) glucose-stimulated
addition, an extrapancreatic activity which includes insulin secretion from isolated rat pancreatic islets:
both insulin-mimetic and insulin-sensitizing activity The insulin concentration of the control group was Results of the current study revealed that vanadyl Glimepiride significantly increased insulin sulfate (15 mg/kg, i.p.) showed a significant reduction secretion from rat pancreatic islets in presence of 6 in the serum glucose level of STZ-induced diabetic rats. mmol/L glucose. However, vanadyl sulfate did not Similar results have been reported by (Bendayan and significantly affect insulin secretion from rat pancreatic Gingras, 1989; Mongold et al., 1990; Dai et al., 1994; islets in presence of 6 mmol/L glucose. No interaction Poucheret et al., 1995; Ray et al., 2004; Bolkent et al., has been observed when vanadyl sulfate is given with glimepiride. Combination of vanadyl sulfate with However, according to this study the improvement glimepiride did not significantly affect glimepiride- in the serum glucose level induced by vanadyl sulfate induced increase in insulin secretion from rat pancreatic was not accompanied by increase in serum insulin level in STZ-induced diabetic rats. Results of the present study confirm the study of (Brichard et al., 1989; DISCUSSION
Poucheret et al., 1995; Cadene et al., 1996; De Tata In the present study, diabetes was induced by a The effect of vanadyl sulfate on in vivo insulin single injection of streptozotocin (50 mg/kg, i.p.) which secretion of this study is also confirmed by the in vitro was reported to increase blood glucose level and study (isolated rat pancreatic islets), where data of the decrease insulin sensitivity index, that are the main present investigation revealed that vanadyl sulfate (1 characteristics of type II diabetes mellitus (Niu et al., µmol/L) inhibited glucose (6 mmol/L)-stimulated insulin secretion from isolated rat pancreatic islets. Findings of the current study revealed that These results are consistent with the data given by glimepiride (10 mg/kg) significantly reduced the serum glucose level of STZ-induced diabetic rats after two Depending on the aforementioned findings of this weeks of daily dose administration. This result is in study, it could be suggested that the hypoglycemic accordance with that of (Mir et al., 2008; Hsu et al., action vanadyl sulfate is most probably attributed to its insulin-mimetic effects, which has been observed by In addition, glimepiride significantly elevated (Siddiqui et al., 2005; Wilsey et al., 2006) or to its serum insulin level in STZ-diabetic rats. This result is insulin-sensitizing effect as reported by (Cohen et al., in total agreement with that of (Rosenstock et al., 1996; 1995; Fantus and Tsiani, 1998; Cam et al., 1999; Korytkowski et al., 2002; Hsu et al., 2009). The Verma et al., 1998). This insulin-sensitizing action of aforementioned in vivo results were also supported by the in vitro results that glimepiride (10 µmol/L) vanadium might be attributed to its inhibitory effect of significantly increased glucose (6 mmol/L)-stimulated Protein Tyrosine Phosphatases (PTPs) (Sakurai et al., insulin secretion from isolated rat pancreatic islets. 2006) particularly PTP1B, whose inhibition will lead to Similarly, (Hsu et al., 2009) found that glimepiride stimulation of insulin receptors (Ramachandran et al., stimulated insulin release from rat pancreatic islets. 1992; Ahmad et al., 1995; Seely et al., 1996; Depending on the findings of the present study, it Bandyopadhyay et al., 1997; Wang et al., 2001). could be suggested that the hypoglycemic effect of Concerning the liver glycogen content, results of glimepiride was attributed to its stimulation of insulin this study have demonstrated that the diabetic control secretion. This explanation is in accordance with that group showed a significant decrease in liver glycogen given by (Philipson and Steiner, 1995; Fuhlendorff content after STZ injection. Similar results were et al., 1998; Muller, 2005) who found that glimepiride obtained by (Rashwan and Al-Firdous, 2011). binds to sulfonylurea receptors on β-cells leading to Glimepiride, in a dose of 10 mg/kg, significantly increased liver glycogen content of STZ-diabetic rats. calcium channels and increase in Ca2+ influx leading to This finding is in full agreement with other studies insulin release from pancreatic β-cells. (Muller and Wied, 1993; Muller and Geisen, 1996; In contrast to our results (Duckworth et al., 1972; Muller, 2000; Haupt et al., 2002; Mori et al., 2008). Olefsky and Reaven, 1976; Beck-Nielsen et al., 1979; These results suggest that glimepiride stimulates See et al., 2003) observed that glimepiride has glycogenesis and this confirms the study of (See et al., hypoglycemic action without significant effect on Br. J. Pharmacol. Toxicol., 3(6): 278-288, 2012 This result can be explained by Muller (2000) who Vanadyl sulfate returned the level of serum reported that glimepiride activates insulin receptors and TBARS to the normal value and significantly elevated thereby it can possibly stimulate insulin-induced the blood GSH and SOD levels as compared to the glycogen synthesis. In addition, (Olbrich et al., 1999; diabetic control value. These results are in accordance Reimann et al., 2000) found that sulfonylurea’s inhibit with (Siddiqui et al., 2005; Shukla et al., 2007) for KATP channels and thereby control the intracellular Ca TBARS; (Bolkent et al., 2005; Preet et al., 2005) for concentrations. This regulation of intracellular Ca GSH and (Siddiqui et al., 2005; Shukla et al., 2007) for content can affect the insulin-signaling cascade and thereby stimulates glycogen synthesis (Haupt et al., antioxidant effects of vanayl sulfate may be attributed Vanadyl sulfate normalized the liver glycogen to its ability to normalize the decreased activity of content decreased by STZ. These results are in parallel Na+/K+ ATPase, increased lipid peroxides and altered with the data obtained by Tolman et al. (1979), Niu membrane fluidity caused by diabetes, which in turn et al. (2007) and Rashwan and Al-Firdous (2011). will lead to a decrease in the production of free radicals, The most likely explanation for this action is that vanadium activates the glucose-sensing enzyme, lipid peroxides and restoring the antioxidant enzymes glucokinase, in the liver and pancreas. This explanation activity (Siddiqui et al., 2005). is in agreement with (Niu et al., 2007). This enzyme Finally, according to the findings of the present has been reported to stimulate glucose uptake and study, it could be stated that there is no significant glycogen synthesis in the liver and thereby decrease the interaction between vanadyl sulfate and glimepiride blood glucose level (Efanov et al., 2005). Data of the current study revealed that STZ caused aforementioned parameters. It follows that the two a significant increase in serum TBARS level drugs can be taken together safely without fear of any accompanied by a significant reduction in blood GSH serious reactions. The absence of additive action and SOD levels. These results are in harmony with that between the two drugs observed in this study may be of (El-Missiry et al., 2004; Preet et al., 2005; Siddiqui attributed to the use of doses which give maximal et al., 2005; Shukla et al., 2007) for TBARS; (Yarat response, thus no potentiating of action was observed. et al., 2001; Bolkent et al., 2005; Preet et al., 2005; Kakadiya et al., 2010) for GSH and (Siddiqui et al., REFERENCES
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