Abstract
The therapeutic potential of molecular hydrogen (H 2) is emerging in a number of human diseases and in their animal models, including in particular Parkinson's disease (PD). H2 supplementation of drinking water has been shown to exert disease-modifying effects in PD patients and neuroprotective effects in experimental PD model mice. However, H2 supplementation does not result in detectable changes in striatal H 2 levels, indicating an indirect effect. Here we show that H2 supplementation increases gastric expression of mRNA encoding ghrelin, a growth hormone secretagogue, and ghrelin secretion, which are antagonized by the β 1-adrenoceptor blocker, atenolol. Strikingly, the neuroprotective effect of H 2 water was abolished by either administration of the ghrelin receptor-antagonist, D-Lys 3 GHRP-6, or atenolol. Thus, the neuroprotective effect of H2 in PD is mediated by enhanced production of ghrelin. Our findings point to potential, novel strategies for ameliorating pathophysiology in which a protective effect of H2 supplementation has been demonstrated.
| Original language | English |
|---|---|
| Article number | 3273 |
| Journal | Scientific reports |
| Volume | 3 |
| DOIs | |
| Publication status | Published - Nov 29 2013 |
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Oral 'hydrogen water' induces neuroprotective ghrelin secretion in mice. / Matsumoto, Akio; Yamafuji, Megumi; Tachibana, Tomoko; Nakabeppu, Yusaku; Noda, Mami; Nakaya, Haruaki.
In: Scientific reports, Vol. 3, 3273, 29.11.2013.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Oral 'hydrogen water' induces neuroprotective ghrelin secretion in mice
AU - Matsumoto, Akio
AU - Yamafuji, Megumi
AU - Tachibana, Tomoko
AU - Nakabeppu, Yusaku
AU - Noda, Mami
AU - Nakaya, Haruaki
PY - 2013/11/29
Y1 - 2013/11/29
N2 - The therapeutic potential of molecular hydrogen (H 2) is emerging in a number of human diseases and in their animal models, including in particular Parkinson's disease (PD). H2 supplementation of drinking water has been shown to exert disease-modifying effects in PD patients and neuroprotective effects in experimental PD model mice. However, H2 supplementation does not result in detectable changes in striatal H 2 levels, indicating an indirect effect. Here we show that H2 supplementation increases gastric expression of mRNA encoding ghrelin, a growth hormone secretagogue, and ghrelin secretion, which are antagonized by the β 1-adrenoceptor blocker, atenolol. Strikingly, the neuroprotective effect of H 2 water was abolished by either administration of the ghrelin receptor-antagonist, D-Lys 3 GHRP-6, or atenolol. Thus, the neuroprotective effect of H2 in PD is mediated by enhanced production of ghrelin. Our findings point to potential, novel strategies for ameliorating pathophysiology in which a protective effect of H2 supplementation has been demonstrated.
AB - The therapeutic potential of molecular hydrogen (H 2) is emerging in a number of human diseases and in their animal models, including in particular Parkinson's disease (PD). H2 supplementation of drinking water has been shown to exert disease-modifying effects in PD patients and neuroprotective effects in experimental PD model mice. However, H2 supplementation does not result in detectable changes in striatal H 2 levels, indicating an indirect effect. Here we show that H2 supplementation increases gastric expression of mRNA encoding ghrelin, a growth hormone secretagogue, and ghrelin secretion, which are antagonized by the β 1-adrenoceptor blocker, atenolol. Strikingly, the neuroprotective effect of H 2 water was abolished by either administration of the ghrelin receptor-antagonist, D-Lys 3 GHRP-6, or atenolol. Thus, the neuroprotective effect of H2 in PD is mediated by enhanced production of ghrelin. Our findings point to potential, novel strategies for ameliorating pathophysiology in which a protective effect of H2 supplementation has been demonstrated.
UR - http://www.scopus.com/inward/record.url?scp=84888250631&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84888250631&partnerID=8YFLogxK
U2 - 10.1038/srep03273
DO - 10.1038/srep03273
M3 - Article
C2 - 24253616
AN - SCOPUS:84888250631
VL - 3
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 3273
ER -