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  1. C. 医薬保健学域; 医学類・薬学類・医薬科学類・保健学類
  2. c 10. 学術雑誌掲載論文(医・保健)
  3. 1. 査読済論文(医学・保健)

Ectopic fat accumulation in the liver and glucose homeostasis

http://hdl.handle.net/2297/45533
http://hdl.handle.net/2297/45533
519e6ad5-d3fd-4ee0-a56d-8ef29c31fdcb
名前 / ファイル ライセンス アクション
ME-PR-TAKAMURA-T-185.pdf ME-PR-TAKAMURA-T-185.pdf (1.1 MB)
アイテムタイプ 図書 / Book(1)
公開日 2017-10-03
タイトル
タイトル Ectopic fat accumulation in the liver and glucose homeostasis
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_2f33
資源タイプ book
著者 Takamura, Toshinari

× Takamura, Toshinari

WEKO 225
e-Rad 00324111
金沢大学研究者情報 00324111
研究者番号 00324111

Takamura, Toshinari

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Misu, Hirofumi

× Misu, Hirofumi

WEKO 520
金沢大学研究者情報 80447680
研究者番号 80447680

Misu, Hirofumi

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Kaneko, Shuichi

× Kaneko, Shuichi

WEKO 62
e-Rad 60185923
金沢大学研究者情報 60185923
研究者番号 60185923

Kaneko, Shuichi

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書誌情報 Musculoskeletal Disease Associated with Diabetes Mellitus

p. 185-199, 発行日 2016-01-01
ISBN
関連タイプ isIdenticalTo
識別子タイプ ISBN
関連識別子 978-443155720-3
ISBN
関連タイプ isIdenticalTo
識別子タイプ ISBN
関連識別子 978-443155719-7
抄録
内容記述タイプ Abstract
内容記述 Liver fat is associated not only with enhanced hepatic glucose production but also with skeletal muscle insulin resistance, supporting a central role of fatty liver in systemic insulin resistance and existence of a network between the liver and skeletal muscle. Palmitate and cholesterol act as toxic lipids to cause hepatic insulin resistance via mitochondria-derived oxidative stress. Obesity-mediated disruption in crosstalk among protein-, glucose- and lipid-metabolism pathways results in hepatic insulin resistance, enhanced gluconeogenesis and liver steatosis by impairing proteasome function. The liver plays as an endocrine organ to produce functional hepatokines and thereby mediates fatty liver-associated skeletal muscle insulin resistance through unique mechanisms. Selenoprotein P is upregulated through FoxOs and hyperglycemia and causes resistance to insulin, angiogenesis and exercise through reductive stress. LECT2 is upregulated in satiety through AMPK inactivation and contributes to the development of muscle insulin resistance and obesity by activating JNK and by impairing myogenesis, respectively. Therefore, overnutrition evokes remodeling of nutrient homeostasis by toxic lipids and proteasome dysfunction in the liver. The remodeling also results in the overproduction of hepatokines that disrupt inter-organ network leading to pathology of diabetes. © Springer Japan 2016.
内容記述
内容記述タイプ Other
内容記述 Book Chapter / Embargo Period 12 months
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
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