{"_buckets": {"deposit": "9928b108-4a3b-4a61-bacb-b9b6b8a9815c"}, "_deposit": {"id": "49126", "owners": [], "pid": {"revision_id": 0, "type": "depid", "value": "49126"}, "status": "published"}, "_oai": {"id": "oai:tsukuba.repo.nii.ac.jp:00049126"}, "item_5_biblio_info_6": {"attribute_name": "\u66f8\u8a8c\u60c5\u5831", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2018-11", "bibliographicIssueDateType": "Issued"}, "bibliographicIssueNumber": "4", "bibliographicPageEnd": "516", "bibliographicPageStart": "509", "bibliographicVolumeNumber": "67", "bibliographic_titles": [{"bibliographic_title": "Experimental animals"}]}]}, "item_5_description_4": {"attribute_name": "\u6284\u9332", "attribute_value_mlt": [{"subitem_description": "Mitochondrial DNA (mtDNA) mutator mice showing accelerated accumulation of mtDNA with somatic mutations are potentially useful models of human aging, whereas mito-mice\u0394 showing accelerated accumulation of mtDNA with a deletion mutation (\u0394mtDNA) are potentially useful models of mitochondrial diseases but not human aging, even though both models express an age-associated decrease in mitochondrial respiration. Because osteoporosis is the only premature aging phenotype observed in mtDNA mutator mice with the C57BL/6J nuclear genetic background, our previous study precisely examined its expression spectra and reported that both mtDNA mutator mice and mito-mice\u0394, but not aged mice, developed decreased cortical bone thickness. Moreover, decreased cortical bone thickness is usually not seen in aged humans but is commonly seen in the patients with hyperparathyroidism caused by oversecretion of parathyroid hormone (PTH). In the present study, we showed higher concentrations of blood PTH in mtDNA mutator mice and mito-mice\u0394 than in aged mice. We also found that both models developed decreased mitochondrial respiration in the duodenum or renal tubules, which would lead to hypocalcemia, oversecretion of PTH, and ultimately osteoporosis. Thus, mtDNA mutator mice and mito-mice\u0394 may be useful models of human osteoporosis caused not by aging but by hyperparathyroidism.", "subitem_description_type": "Abstract"}]}, "item_5_publisher_27": {"attribute_name": "\u51fa\u7248\u8005", "attribute_value_mlt": [{"subitem_publisher": "Japanese Association for Laboratory Animal Science"}]}, "item_5_relation_11": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_type_id": {"subitem_relation_type_id_text": "10.1538/expanim.18-0060", "subitem_relation_type_select": "DOI"}}]}, "item_5_relation_9": {"attribute_name": "\u66f8\u8a8c\u30ec\u30b3\u30fc\u30c9ID", "attribute_value_mlt": [{"subitem_relation_type_id": {"subitem_relation_type_id_text": " AA11032321", "subitem_relation_type_select": "NCID"}}]}, "item_5_rights_12": {"attribute_name": "\u6a29\u5229", "attribute_value_mlt": [{"subitem_rights": "\u00a92018 Japanese association for Laboratory animal Science"}, {"subitem_rights": "This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License \u003chttp://creativecommons.org/licenses/by-nc-nd/4.0/\u003e."}]}, "item_5_select_15": {"attribute_name": "\u8457\u8005\u7248\u30d5\u30e9\u30b0", "attribute_value_mlt": [{"subitem_select_item": "publisher"}]}, "item_5_source_id_7": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "1341-1357", "subitem_source_identifier_type": "ISSN"}]}, "item_creator": {"attribute_name": "\u8457\u8005", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "\u4e2d\u7530, \u548c\u4eba"}, {"creatorName": "\u30ca\u30ab\u30c0, \u30ab\u30ba\u30c8", "creatorNameLang": "ja-Kana"}, {"creatorName": "NAKADA, Kazuto", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106732", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "80323244", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": 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"resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_title": "Mito-mice\u2206 and mitochondrial Mito-mice\u2206 and mitochondrial DNA mutator mice as models of human osteoporosis caused not by aging but by hyperparathyroidism", "item_titles": {"attribute_name": "\u30bf\u30a4\u30c8\u30eb", "attribute_value_mlt": [{"subitem_title": "Mito-mice\u2206 and mitochondrial Mito-mice\u2206 and mitochondrial DNA mutator mice as models of human osteoporosis caused not by aging but by hyperparathyroidism"}]}, "item_type_id": "5", "owner": "1", "path": ["160/849", "3/62/5587/1335"], "permalink_uri": "http://hdl.handle.net/2241/00154598", "pubdate": {"attribute_name": "\u516c\u958b\u65e5", "attribute_value": "2019-02-14"}, "publish_date": "2019-02-14", "publish_status": "0", "recid": "49126", "relation": {}, "relation_version_is_last": true, "title": ["Mito-mice\u2206 and mitochondrial Mito-mice\u2206 and mitochondrial DNA mutator mice as models of human osteoporosis caused not by aging but by hyperparathyroidism"], "weko_shared_id": 5}