12 research outputs found

    Effect of iron on pancreatic beta cell function and insulin resistance in female albino rats

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    Background: Increase in total body iron store has been reported in the aetiology and development of diabetes mellitus. The effect of iron supplementation in female with respect to the incidence of diabetes mellitus was investigated on the pancreatic beta cell function and insulin resistance in normal female rats. Methods: Forty-eight Wistar rats (150-200g) were divided into 6 groups as follows; Group 1 (control) received 0.3ml distilled water, groups 2, 3, 4, 5 and 6 received iron (10mg/kg, 20mg/kg, 40mg/kg, 80mg/kg and 160mg/kg respectively) daily for 12days. Blood from the tail vein of each animal was assessed for blood glucose level on days 0, 3, 6 and 12 using glucometer. At 12 days post iron treatment, blood (3ml) was obtained from the retro-orbital sinus of each animal and allowed to coagulate. Serum obtained was analysed for insulin concentration using ELISA method. Histopathology of the pancreas was assessed using Hematoxylin and Eosin technique. Data were expressed as Mean ± SEM and analyzed using two-way ANOVA at P<0.05. Results: Blood glucose level, insulin concentration, insulin resistance and pancreatic beta cell function increased significantly with increased concentration of iron. Histology of the pancreas showed fat infiltration of both acini and islets with increased iron concentration. Mild inflammation of the islets was observed at 160mg/kg. Conclusion: Administration of iron at 40mg/kg and above in female rats caused hyperglycaemia, insulin resistance, hyperinsulinaemia, inflammation and pancreatic beta cell dysfunction thus predisposing the animal to type 2 diabetes mellitus.Keywords: Iron, Hyperglycaemia, Insulin resistance, Hyperinsulinaemia, inflammation, Beta cell dysfunction

    Association between erythrocyte Na+K+-ATPase activity and some blood lipids in type 1 diabetic patients from Lagos, Nigeria

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    <p>Abstract</p> <p>Background</p> <p>Altered levels of erythrocyte Na<sup>+</sup>K<sup>+</sup>-ATPase, atherogenic and anti-atherogenic lipid metabolites have been implicated in diabetic complications but their pattern of interactions remains poorly understood.</p> <p>This study evaluated this relationship in Nigerian patients with Type 1 diabetes mellitus.</p> <p>Methods</p> <p>A total of 34 consented Type 1 diabetic patients and age -matched 27 non-diabetic controls were enrolled. Fasting plasma levels of total cholesterol, triglycerides and HDL-cholesterol were determined spectrophotometrically and LDL-cholesterol estimated using Friedewald formula. Total protein content and Na+K+-ATPase activity were also determined spectrophotometrically from ghost erythrocyte membrane prepared by osmotic lysis.</p> <p>Results</p> <p>Results indicate significant (P < 0.05) reduction in Na<sup>+</sup>K<sup>+</sup>-ATPase activity in the Type 1 diabetic patients (0.38 ± 0.08 vs. 0.59 ± 0.07 uM Pi/mgprotein/h) compared to the control but with greater reduction in the diabetic subgroup with poor glycemic control (n = 20) and in whom cases of hypercholesterolemia (8.8%), hypertriglyceridemia (2.9%) and elevated LDL-cholesterol (5.9% each) were found. Correlation analyses further revealed significant (P < 0.05) inverse correlations [r = -(0.708-0.797] between all the atherogenic lipid metabolites measured and Na<sup>+</sup>K<sup>+</sup>-ATPase in this subgroup contrary to group with good glycemic control or non-diabetic subjects in which significant (P < 0.05) Na<sup>+</sup>K<sup>+</sup>-ATPase and HDL-C association were found (r = 0.427 - 0.489). The Na<sup>+</sup>K<sup>+</sup>-ATPase from the diabetic patients also exhibited increased sensitivity to digoxin and alterations in kinetic constants Vmax and Km determined by glycemic status of the patients.</p> <p>Conclusion</p> <p>It can be concluded that poor glycemic control evokes greater reduction in erythrocyte Na<sup>+</sup>K<sup>+</sup>-ATPase activity and promote enzyme-blood atherogenic lipid relationships in Type 1 diabetic Nigerian patients.</p

    Effect of Magnesium pre-treatment on Alloxan induced hyperglycemia in rats

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    Background: The role of vitamins and mineral supplementation in the prevention of diabetes mellitus is not well elucidated.Objective: The effect of prior administration of magnesium on alloxan induced diabetes was assessed in rats.Methods: 36 Male albino rats were used for this study. The animals were divided into 6 groups of 6 animals each; group 1 was healthy control; groups 2 served as diabetic control. Animals in group 3 received magnesium (100 mg/kg) i.p one hour prior to alloxan (120 mg/kg) administration, group 4 were also received magnesium (150 mg/kg) i.p one hour prior to alloxan administration. Animals in group 5 received magnesium (100 mg/kg) i.p only; group 6 animals received magnesium(150 mg/kg) i.p only. Blood samples were obtained from all animals and plasma glucose levels were determined on Day 0 (prior to treatment), Day 2, Day 5, Day 7 and Day 10 after the commencement of treatment.Results: There was significant increase (

    Effect of Magnesium pre-treatment on Alloxan induced hyperglycemia in rats

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    Background: The role of vitamins and mineral supplementation in the prevention of diabetes mellitus is not well elucidated. Objective: The effect of prior administration of magnesium on alloxan induced diabetes was assessed in rats. Methods: 36 Male albino rats were used for this study. The animals were divided into 6 groups of 6 animals each; group 1 was healthy control; groups 2 served as diabetic control. Animals in group 3 received magnesium (100 mg/kg) i.p one hour prior to alloxan (120 mg/kg) administration, group 4 were also received magnesium (150 mg/kg) i.p one hour prior to alloxan administration. Animals in group 5 received magnesium (100 mg/kg) i.p only; group 6 animals received magnesium (150 mg/kg) i.p only. Blood samples were obtained from all animals and plasma glucose levels were determined on Day 0 (prior to treatment), Day 2, Day 5, Day 7 and Day 10 after the commencement of treatment. Results: There was significant increase (P<0.001) in plasma glucose values in the alloxan treated group when compared with the control values. There was also a significant increase (P<0.01) in plasma glucose levels in the magnesium-pretreated (100 mg/kg and 150 mg/kg) diabetic groups when compared with healthy controls whereas there was a significant reduction (P<0.01) in plasma glucose level when compared with the diabetic control. Conclusion: This study has shown that magnesium pretreatment may delay the onset and subsequently cause a reduction in hyperglycemia in alloxan induced diabetes. This effect of magnesium may be attributed to its role as a scavenger of highly reactive hydroxyl radicals generated through alloxan reactions, its potentiation of glutathione antioxidant production and its role as a calcium blocker
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