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  1. 学術雑誌論文
  2. 琉球医学会
  3. 琉球医学会誌
  4. 29巻1・2号
  1. 部局別インデックス
  2. その他

[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/20.500.12000/0002016231
48638855-9c74-4df9-8e79-9c626841a7f4
名前 / ファイル ライセンス アクション
v29p15.pdf 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
作成者 益崎, 裕章

× 益崎, 裕章

ja 益崎, 裕章

Masuzaki, Hiroaki

× Masuzaki, Hiroaki

en 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
言語 en
主題Scheme Other
主題 adipose tissue
言語 en
主題Scheme Other
主題 leptin
言語 en
主題Scheme Other
主題 AMPK
言語 en
主題Scheme Other
主題 type 4 melanocortin receptor (MC 4R)
言語 en
主題Scheme Other
主題 glucocorticoid
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
収録物識別子タイプ ISSN
収録物識別子 0289-1530
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
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