| 研究実績の概要 |
Zinc is an essential mineral that plays an important role in the body. We previously reported that orally feeding zinc-enriched yeast to mice induces non-rapid-eye-movement sleep. In addition, astaxanthin, an antioxidant abundant in seafood such as salmon and krill, is able to chelate minerals and may promote zinc absorption, which in return may also improve sleep. The purpose of our study was to examine the effect of zinc-rich and astaxanthin-containing food on sleep in humans.
We conducted a randomized, double-blinded, placebo-controlled parallel group trial of 120 healthy subjects and recorded their night activity by actigraphy for 12 weeks. These subjects were divided into 4 groups: placebo, zinc-rich food, zinc- and astaxanthin-rich food, and placebo supplemented with zinc-enriched yeast and astaxanthin oil. Compared with the placebo group, the zinc-rich food group efficiently decreased the time necessary to fall asleep and improved sleep efficiency, whereas the group that ingested zinc-enriched yeast and astaxanthin oil significantly improved the sleep onset latency. Actigraphic sleep monitoring demonstrated that eating zinc-rich food improved sleep onset latency as well as improved the sleep efficiency in healthy individuals. We then focussed on designing a new improved food supplement to promote sleep. It was released on the market as Oxybarrier Suttone Rich by Fujifilm Healthcare Corporation.
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| 現在までの達成度 (区分) |
現在までの達成度 (区分)
2: おおむね順調に進展している
理由
We performed experiments in order to understand the molecular mechanisms involved in the regulation of zinc-induced sleep. We observed an increase of neuronal activation into the bed nucleus of the stria terminalis (BNST) following zinc administration. We stereotaxically injected AAVs expressing mutant G protein coupled receptors that respond to otherwise inert compounds to activate (hM3Dq) or inactivate (hM4Di) G protein signaling of neurons into the zinc controlled brain region and activated the infected neurons by administering CNO. Neuronal activation of hM3Dq neurons could efficiently increase non-REM sleep, while the activation of hM4Di could efficiently inhibit the sleep inducing effects of zinc. Together, these results demonstrate the essential role of these neurons in the control of zinc-induced sleep.
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| 今後の研究の推進方策 |
We will continue to determine the molecular mechanisms involved in the regulation of sleep by zinc. To do so, we will control the activity of zinc-sensitive neurons by optogenetics, which offers a better temporal control of activation/inhibition compared to the CNO/DREADD system.
We will also characterize the identity of the zinc responding neurons by in situ hybridization for neuronal markers.
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