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Front Neurosci. 2018 Oct 2;12:679. doi: 10.3389/fnins.2018.00679. eCollection 2018.

Adiponectin Mediates Running-Restored Hippocampal Neurogenesis in Streptozotocin-Induced Type 1 Diabetes in Mice.

Yau SY1, Lee TH1, Li A2, Xu A3,4,5, So KF2,6,7.

Author information

1
Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hung Hom, Hong Kong.
2
Guangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, China.
3
Department of Medicine, The University of Hong Kong, Pokfulam, Hong Kong.
4
Department of Pharmacology and Pharmacy, The University of Hong Kong, Pokfulam, Hong Kong.
5
The State Key Laboratory of Pharmacology, The University of Hong Kong, Pokfulam, Hong Kong.
6
State Key Laboratory of Brain and Cognitive Sciences, Pokfulam, Hong Kong.
7
Department of Ophthalmology, The University of Hong Kong, Pokfulam, Hong Kong.

Abstract

Streptozotocin (STZ)-induced diabetes impairs learning and memory performance and reduces adult hippocampal neurogenesis. Physical exercise brings beneficial effects. We have previously shown that adiponectin, an adipocyte-secreted hormone critically involved in the pathology of diabetes, is a key mediator for exercise-enhanced adult hippocampal neurogenesis. Here, we tested whether adiponectin is required for exercise to restore adult hippocampal neurogenesis in an animal model of diabetes. The findings showed that a single injection of 195 mg/kg STZ-induced diabetes significantly increased serum levels of corticosterone and reduced hippocampal adiponectin levels in adult mice. STZ injection also significantly reduced the number of Ki67 and doublecortin (DCX) positive cells and the ratio of co-labeling of DCX and bromodeoxyuridine (BrdU) in the hippocampal dentate region, indicating a decrease in adult hippocampal neurogenesis. Two-week voluntary wheel running significantly restored hippocampal neurogenesis in the diabetic wild-type mice, but not adiponectin knockout mice, indicating that adiponectin is critical for physical exercise to restore hippocampal adult neurogenesis in mice with diabetes. The results suggest that increasing adiponectin levels could be a therapeutic approach to restore hippocampal neurogenesis impairment in individuals with diabetes.

KEYWORDS:

adiponectin; hippocampal neurogenesis; physical exercise; streptozotocin; type I Diabetes

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