Bina Kumari Mehta1, Kaushal Kumar Singh2, Sugato Banerjee1. 1. a Department of Pharmaceutical Sciences and Technology , Birla Institute of Technology , Ranchi , India. 2. b Department of Veterinary Pathology, Faculty of Veterinary Science & Animal Husbandry , Birsa Agriculture University , Ranchi , India.
Abstract
OBJECTIVES: Type 2 diabetes (T2D)-associated cognitive impairment is highly prevalent especially among the geriatric population. Here, we investigate the role of exercise in T2D-associated cognitive decline in rats. METHODS: T2D was induced using high-fat diet (15 days) followed by low-dose STZ (25mg/kg). The T2D animals were subjected to aerobic exercise on running wheel for 6 weeks. Effect of aerobic exercise on cognitive performance of T2D animals was measured using step-down and transfer latency tests. This was followed by the measurement of reduced glutathione levels in hippocampal homogenates. We also measured hippocampal AchE activity and levels of neuroinflammatory markers such as IL-1 β, TNF-α and MCP-1. Morphology and density of hippocampal neurons were also determined by histopathological studies. RESULTS: Exercise led to the following changes in T2D animals. It led to decrease in fasting blood glucose level (<250 mg/kg) and HbA1c (8.5 ± 0.23) compared to diabetic (11.73 ± 0.14) animals and improved insulin resistance. There was an increase in step-down latency (p < 0.001) and a decrease in transfer latency (p < 0.01) suggesting improved cognitive function. A significant increase in GSH levels (1.828 ± 0.024) compared to diabetic group (1.52 ± 0.03; p < 0.001) and decrease in AchE activity (1.4 ± 0.05) compared to diabetic group (1.65 ± 0.03; p < 0.05) were also observed. It reduced the levels of neuroinflammatory markers such as IL-1β, TNF-α and MCP-1 (p < 0.01). Hippocampal sections showed higher CA1 and CA3 neuronal density (p < 0.001) than T2D group. CONCLUSION: We may conclude that aerobic exercise could partially reverse diabetes-associated cognitive decline by reducing oxidative stress and inflammatory milieu in T2D animal brain.
OBJECTIVES:Type 2 diabetes (T2D)-associated cognitive impairment is highly prevalent especially among the geriatric population. Here, we investigate the role of exercise in T2D-associated cognitive decline in rats. METHODS: T2D was induced using high-fat diet (15 days) followed by low-dose STZ (25mg/kg). The T2D animals were subjected to aerobic exercise on running wheel for 6 weeks. Effect of aerobic exercise on cognitive performance of T2D animals was measured using step-down and transfer latency tests. This was followed by the measurement of reduced glutathione levels in hippocampal homogenates. We also measured hippocampal AchE activity and levels of neuroinflammatory markers such as IL-1 β, TNF-α and MCP-1. Morphology and density of hippocampal neurons were also determined by histopathological studies. RESULTS: Exercise led to the following changes in T2D animals. It led to decrease in fasting blood glucose level (<250 mg/kg) and HbA1c (8.5 ± 0.23) compared to diabetic (11.73 ± 0.14) animals and improved insulin resistance. There was an increase in step-down latency (p < 0.001) and a decrease in transfer latency (p < 0.01) suggesting improved cognitive function. A significant increase in GSH levels (1.828 ± 0.024) compared to diabetic group (1.52 ± 0.03; p < 0.001) and decrease in AchE activity (1.4 ± 0.05) compared to diabetic group (1.65 ± 0.03; p < 0.05) were also observed. It reduced the levels of neuroinflammatory markers such as IL-1β, TNF-α and MCP-1 (p < 0.01). Hippocampal sections showed higher CA1 and CA3 neuronal density (p < 0.001) than T2D group. CONCLUSION: We may conclude that aerobic exercise could partially reverse diabetes-associated cognitive decline by reducing oxidative stress and inflammatory milieu in T2D animal brain.