WEKO3
アイテム
{"_buckets": {"deposit": "235131be-1e77-47ef-b618-2acae54f0af7"}, "_deposit": {"id": "2016231", "owners": [1], "pid": {"revision_id": 0, "type": "depid", "value": "2016231"}, "status": "published"}, "_oai": {"id": "oai:u-ryukyu.repo.nii.ac.jp:02016231", "sets": ["1642838226739", "1642838412624"]}, "author_link": [], "item_1617186331708": {"attribute_name": "Title", "attribute_value_mlt": [{"subitem_1551255647225": "[依頼総説]ヒトは なぜ 太ってしまうのか? -脂肪細胞科学の進歩が拓く 肥満の病態解明と治療の展望-", "subitem_1551255648112": "ja"}, {"subitem_1551255647225": "Recent Research Progress in Molecular Pathophysiology of Obesity-Diabetes Syndrome", "subitem_1551255648112": "en"}]}, "item_1617186419668": {"attribute_name": "Creator", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "益崎, 裕章", "creatorNameLang": "ja"}]}, {"creatorNames": [{"creatorName": "Masuzaki, Hiroaki", "creatorNameLang": "en"}]}]}, "item_1617186476635": {"attribute_name": "Access Rights", "attribute_value_mlt": [{"subitem_1522299639480": "open access", "subitem_1600958577026": "http://purl.org/coar/access_right/c_abf2"}]}, "item_1617186499011": {"attribute_name": "Rights", "attribute_value_mlt": [{"subitem_1522650717957": "ja", "subitem_1522651041219": "琉球医学会"}]}, "item_1617186609386": {"attribute_name": "Subject", "attribute_value_mlt": [{"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "obesity"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "adipose tissue"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "leptin"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "AMPK"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "type 4 melanocortin receptor (MC 4R)"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "glucocorticoid"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "11 beta-hydroxysteroid dehydrogenase type 1"}]}, "item_1617186626617": {"attribute_name": "Description", "attribute_value_mlt": [{"subitem_description": "A variety of molecular events provoked in obese adipose tissue considerably contribute to the pathophysiology of life style-related metabolic diseases. Adipocyte-derived hormone leptin controls appetite and fuel homeostasis via the hypothalamus. However, clinical application of leptin for the treatment of obesity-diabetes syndrome has been hampered by the fact that leptin action is deteriorated on a high-fat, westernized diet. In this context, we previously found that the activity of AMP-activated protein kinase (AMPK), a key player of fatty acid oxidation in skeletal muscle, correlates with the increased hypothalamic leptin sensitivity and metabolic phenotype in transgenic mice overexpressing leptin. Intracerebroventricular administration of type 4 melanocortin receptor agonist robustly overcomes high fat diet-induced leptin resistance and ameliorates fuel dyshomeostasis and hyperphagia in mice, with a concomitant recovery of AMPK activity. On the other hand, glucocorticoid regulates adipose tissue metabolism and body fat distribution, and its action on target tissues depends not only on circulating level but on intracellular concentrations. Locally-enhanced action of glucocorticoid in adipose tissue via the intracellular glucocorticoid reactivating enzyme, 11β-hydrox ysteroid dehydrogenase type 1 (11β-HSD 1) contributes to dysfunction of adipose tissue. Adipose-specific 11β-HSD 1 overexpressors exemplify visceral fat accumulation with insulin resistance, dyslipidemia and hypertension. In contrast, 11β-HSD 1 systemic knockouts as well as adipose-specific 11β-HSD2 transgenics (where intracellular glucocorticoid reactivation was suppressed exclusively in adipose tissue) protect against diabetes and obesity. Exaggerated action of 11β-HSD 1 preferentially in adipose tissue occurs similarly in human obesity. Rodent experiments demonstrate that orallyadministered selective inhibitors of 11β-HSD 1 ameliorate diabetes and arteriosclerosis. These findings offer us the potential for novel therapeutic options in human metabolic diseases.", "subitem_description_type": "Other"}, {"subitem_description": "論文", "subitem_description_type": "Other"}]}, "item_1617186643794": {"attribute_name": "Publisher", "attribute_value_mlt": [{"subitem_1522300295150": "ja", "subitem_1522300316516": "琉球医学会"}]}, "item_1617186702042": {"attribute_name": "Language", "attribute_value_mlt": [{"subitem_1551255818386": "jpn"}]}, "item_1617186920753": {"attribute_name": "Source Identifier", "attribute_value_mlt": [{"subitem_1522646500366": "ISSN", "subitem_1522646572813": "1346-888X"}, {"subitem_1522646500366": "ISSN", "subitem_1522646572813": "0289-1530"}, {"subitem_1522646500366": "NCID", "subitem_1522646572813": "AN10369445"}]}, "item_1617186941041": {"attribute_name": "Source Title", "attribute_value_mlt": [{"subitem_1522650068558": "ja", "subitem_1522650091861": "琉球医学会誌 = Ryukyu Medical Journal"}]}, "item_1617187056579": {"attribute_name": "Bibliographic Information", "attribute_value_mlt": [{"bibliographicIssueNumber": "1・2", "bibliographicPageEnd": "22", "bibliographicPageStart": "15", "bibliographicVolumeNumber": "29"}]}, "item_1617258105262": {"attribute_name": "Resource Type", "attribute_value_mlt": [{"resourcetype": "journal article", "resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_1617265215918": {"attribute_name": "Version Type", "attribute_value_mlt": [{"subitem_1522305645492": "VoR", "subitem_1600292170262": "http://purl.org/coar/version/c_970fb48d4fbd8a85"}]}, "item_1617605131499": {"attribute_name": "File", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_access", "download_preview_message": "", "file_order": 0, "filename": "v29p15.pdf", "future_date_message": "", "is_thumbnail": false, "mimetype": "", "size": 0, "url": {"objectType": "fulltext", "url": "https://u-ryukyu.repo.nii.ac.jp/record/2016231/files/v29p15.pdf"}, "version_id": "7d488680-38fc-4ec6-ad8c-dee59da27a52"}]}, "item_title": "[依頼総説]ヒトは なぜ 太ってしまうのか? -脂肪細胞科学の進歩が拓く 肥満の病態解明と治療の展望-", "item_type_id": "15", "owner": "1", "path": ["1642838226739", "1642838412624"], "permalink_uri": "http://hdl.handle.net/20.500.12000/0002016231", "pubdate": {"attribute_name": "PubDate", "attribute_value": "2011-03-08"}, "publish_date": "2011-03-08", "publish_status": "0", "recid": "2016231", "relation": {}, "relation_version_is_last": true, "title": ["[依頼総説]ヒトは なぜ 太ってしまうのか? -脂肪細胞科学の進歩が拓く 肥満の病態解明と治療の展望-"], "weko_shared_id": -1}
[依頼総説]ヒトは なぜ 太ってしまうのか? -脂肪細胞科学の進歩が拓く 肥満の病態解明と治療の展望-
http://hdl.handle.net/20.500.12000/0002016231
http://hdl.handle.net/20.500.12000/000201623148638855-9c74-4df9-8e79-9c626841a7f4
名前 / ファイル | ライセンス | アクション |
---|---|---|
v29p15.pdf
|
|
Item type | デフォルトアイテムタイプ(フル)(1) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
公開日 | 2011-03-08 | |||||||||
タイトル | ||||||||||
タイトル | [依頼総説]ヒトは なぜ 太ってしまうのか? -脂肪細胞科学の進歩が拓く 肥満の病態解明と治療の展望- | |||||||||
言語 | ja | |||||||||
タイトル | ||||||||||
タイトル | Recent Research Progress in Molecular Pathophysiology of Obesity-Diabetes Syndrome | |||||||||
言語 | en | |||||||||
作成者 |
益崎, 裕章
× 益崎, 裕章
× Masuzaki, Hiroaki
|
|||||||||
アクセス権 | ||||||||||
アクセス権 | open access | |||||||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||
権利情報 | ||||||||||
言語 | ja | |||||||||
権利情報 | 琉球医学会 | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | obesity | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | adipose tissue | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | leptin | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | AMPK | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | type 4 melanocortin receptor (MC 4R) | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | glucocorticoid | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | 11 beta-hydroxysteroid dehydrogenase type 1 | |||||||||
内容記述 | ||||||||||
内容記述タイプ | Other | |||||||||
内容記述 | A variety of molecular events provoked in obese adipose tissue considerably contribute to the pathophysiology of life style-related metabolic diseases. Adipocyte-derived hormone leptin controls appetite and fuel homeostasis via the hypothalamus. However, clinical application of leptin for the treatment of obesity-diabetes syndrome has been hampered by the fact that leptin action is deteriorated on a high-fat, westernized diet. In this context, we previously found that the activity of AMP-activated protein kinase (AMPK), a key player of fatty acid oxidation in skeletal muscle, correlates with the increased hypothalamic leptin sensitivity and metabolic phenotype in transgenic mice overexpressing leptin. Intracerebroventricular administration of type 4 melanocortin receptor agonist robustly overcomes high fat diet-induced leptin resistance and ameliorates fuel dyshomeostasis and hyperphagia in mice, with a concomitant recovery of AMPK activity. On the other hand, glucocorticoid regulates adipose tissue metabolism and body fat distribution, and its action on target tissues depends not only on circulating level but on intracellular concentrations. Locally-enhanced action of glucocorticoid in adipose tissue via the intracellular glucocorticoid reactivating enzyme, 11β-hydrox ysteroid dehydrogenase type 1 (11β-HSD 1) contributes to dysfunction of adipose tissue. Adipose-specific 11β-HSD 1 overexpressors exemplify visceral fat accumulation with insulin resistance, dyslipidemia and hypertension. In contrast, 11β-HSD 1 systemic knockouts as well as adipose-specific 11β-HSD2 transgenics (where intracellular glucocorticoid reactivation was suppressed exclusively in adipose tissue) protect against diabetes and obesity. Exaggerated action of 11β-HSD 1 preferentially in adipose tissue occurs similarly in human obesity. Rodent experiments demonstrate that orallyadministered selective inhibitors of 11β-HSD 1 ameliorate diabetes and arteriosclerosis. These findings offer us the potential for novel therapeutic options in human metabolic diseases. | |||||||||
内容記述 | ||||||||||
内容記述タイプ | Other | |||||||||
内容記述 | 論文 | |||||||||
出版者 | ||||||||||
言語 | ja | |||||||||
出版者 | 琉球医学会 | |||||||||
言語 | ||||||||||
言語 | jpn | |||||||||
資源タイプ | ||||||||||
資源タイプ | journal article | |||||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
出版タイプ | ||||||||||
出版タイプ | VoR | |||||||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
収録物識別子 | ||||||||||
収録物識別子タイプ | ISSN | |||||||||
収録物識別子 | 1346-888X | |||||||||
収録物識別子 | ||||||||||
収録物識別子タイプ | ISSN | |||||||||
収録物識別子 | 0289-1530 | |||||||||
収録物識別子 | ||||||||||
収録物識別子タイプ | NCID | |||||||||
収録物識別子 | AN10369445 | |||||||||
収録物名 | ||||||||||
言語 | ja | |||||||||
収録物名 | 琉球医学会誌 = Ryukyu Medical Journal | |||||||||
書誌情報 |
巻 29, 号 1・2, p. 15-22 |