Abstract
The effects of zinc supplementation on hippocampal neurogenesis in diabetes mellitus have not been studied. Herein, we investigated the effects of zinc plus cyclo-(His-Pro) (ZC) on neurogenesis occurring in the subgranular zone of dentate gyrus after streptozotocin (STZ)-induced diabetes. ZC (27 mg/kg) was administered by gavage once daily for one or six weeks from the third day after the STZ injection, and histological evaluation was performed at 10 (early phase) or 45 (late phase) days after STZ injection. We found that the proliferation of progenitor cells in STZ-induced diabetic rats showed an increase in the early phase. Additionally, ZC treatment remarkably increased the number of neural progenitor cells (NPCs) and immature neurons in the early phase of STZ-induced diabetic rats. Furthermore, ZC treatment showed increased survival rate of newly generated cells but no difference in the level of neurogenesis in the late phase of STZ-induced diabetic rats. The present study demonstrates that zinc supplementation by ZC increases both NPCs proliferation and neuroblast production at the early phase of diabetes. Thus, this study suggests that zinc supplemented with a histidine/proline complex may have beneficial effects on neurogenesis in patients experiencing the early phase of Type 1 diabetes.
Highlights
Type 1 diabetes is reported to make up approximately 5%–10% of the total diabetic population and represents a very significant risk to public health
We examined the effects of zinc plus cyclo-(His-Pro) (ZC) treatment on body weight and blood glucose level in rats that had undergone STZ-induced diabetes during our experimental period (i.e., early (10 days) or late (45 days) diabetic phase)
We found that progenitor cell proliferation in the hippocampus of diabetic rats showed an increase in the early phase after STZ injection
Summary
Type 1 diabetes is reported to make up approximately 5%–10% of the total diabetic population and represents a very significant risk to public health. Cognitive deficits recognized in type 1 diabetes patients include reduced information processing speeds [1,2] and worsening psychomotor function [1,3]. The mechanism by which type 1 diabetes patients develop cognitive dysfunction is not clear. Our previous studies have demonstrated that zinc, an essential trace element, is involved in hippocampal neurogenesis with or without brain injury. Our lab demonstrated that continuous free zinc release from degenerating DG cells may perpetually produce a signal that drives progenitor cell proliferation and aids the survival of neuroblasts following hypoglycemia [11], epilepsy [12], and traumatic brain injury [13]. We recently demonstrated that increasing hippocampal vesicular zinc by zinc supplemented with a histidine/proline complex (zinc plus cyclo-(His-Pro) (ZC)) promotes hippocampal neurogenesis under physiological conditions [14]
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