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Diabetes-induced decrease in rat brain microsomal Ca2+-ATPase activity
Bilgehan Doğru Pekiner1, Net Daş Evcimen, Serpil Nebioğlu
1Department of Biochemistry, Faculty of Pharmacy, University of Ankara, Tandoğan, Turkey.
Abstract:
The Ca(2+)-ATPase activity of rat brain microsomes was studied in streptozotocin (STZ)-induced diabetes. Male rats, 200-250 g, were rendered diabetic by injection of STZ (45 mg kg(-1) body weight) via the teil vein. Brain tissues were collected at 1, 4 and 10 weeks after diabetes was induced for determination of Ca(2+)-ATPase activity, lipid peroxidation and tissue calcium levels. Diabetic rats had significantly elevated blood glucose levels compared to controls. Blood glucose levels were 92.92 +/- 1.22 mg dl(-1) (mean +/- SEM) for the control group, 362.50 +/- 9.61 mg dl(-1) at 1 week and >500 mg dl(-1) at 4, 8 and 10 weeks for the diabetics. Enzyme activities were significantly decreased at 1, 4, 8 and 10 weeks of diabetes relative to the control group (p < 0.001). Ca(2+)-ATPase activity was 0.084 +/- 0.008 U l(-1), 0.029 +/- 0.005 U l(-1), 0.029 +/- 0.006 U l(-1), 0.033 +/- 0.003 U l(-1) and 0.058 +/- 0.006 U l(-1) (mean +/- SEM) at control, 1, 4, 8 and 10 week of diabetes respectively. The change in calcium levels in diabetic rat brain at 8 and 10 weeks of diabetes was significantly higher than that of the control group (p < 0.05). On the other hand lipid peroxidation measured as TBARS (thiobarbituric acid reactive substances) was significantly higher at 8 and 10 weeks of diabetes (p < 0.05). The increase in lipid peroxidation observed in diabetic rat brain may be partly responsible for the decrease in calcium ATPase activity.
Insights
Streptozotocin-induced diabetes in rats significantly decreased brain Ca(2+)-ATPase activity and increased lipid peroxidation and calcium levels. These changes suggest impaired brain function in diabetes.
Area of Science:
- Biochemistry
- Neuroscience
- Endocrinology
Background:
- Diabetes mellitus is a metabolic disorder with potential neurological complications.
- Calcium homeostasis is crucial for neuronal function.
- Ca(2+)-ATPase is a key enzyme regulating calcium levels in brain cells.
Purpose of the Study:
- To investigate the impact of streptozotocin-induced diabetes on Ca(2+)-ATPase activity in rat brain microsomes.
- To assess changes in lipid peroxidation and tissue calcium levels in the brains of diabetic rats.
Main Methods:
- Diabetes was induced in male rats using streptozotocin (STZ).
- Brain tissues were collected at 1, 4, 8, and 10 weeks post-induction.
- Ca(2+)-ATPase activity, lipid peroxidation (TBARS), and tissue calcium levels were measured.
Main Results:
- Diabetic rats exhibited significantly elevated blood glucose levels compared to controls.
- A significant decrease in brain Ca(2+)-ATPase activity was observed at all measured time points in diabetic rats.
- Increased lipid peroxidation and elevated tissue calcium levels were noted in diabetic rat brains at later time points (8 and 10 weeks).
Conclusions:
- Streptozotocin-induced diabetes leads to a marked reduction in brain Ca(2+)-ATPase activity.
- Increased lipid peroxidation may contribute to the observed decrease in Ca(2+)-ATPase activity in diabetic rat brains.
- These biochemical alterations suggest potential mechanisms for neurological dysfunction in diabetes.
