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  1. 教育・研究業績データ
  2. 歯学部

Elevated plasma GLP-1 levels and enhanced expression of cardiac GLP-1 receptors as markers of left ventricular systolic dysfunction: a cross-sectional study.

https://asahi-u.repo.nii.ac.jp/records/2351
https://asahi-u.repo.nii.ac.jp/records/2351
e5d431d3-d761-45d1-9b19-4efd72ff91fc
Item type 朝日大学 教育・研究業績(1)
公開日 2015-02-20
タイトル
タイトル Elevated plasma GLP-1 levels and enhanced expression of cardiac GLP-1 receptors as markers of left ventricular systolic dysfunction: a cross-sectional study.
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_1843
資源タイプ other
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
業績分類
値 学術雑誌論文
教員氏名 竹村, 元三

× 竹村, 元三

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竹村, 元三

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発行、発表雑誌等、又は発表学会等の名称
値 BMJ Open.
巻
値 3
号
値 9
掲載ページ
値 003201
単著、共著の別
値 共著
発行又は発表の年月
日付 2013-09-03
PubMed番号
値 24002982
概要
値 We aimed to elucidate usefulness of plasma glucagon-like peptide-1 (GLP-1) levels for the assessment of left ventricular (LV) dysfunction by examining the relationship among plasma GLP-1 levels, expression of cardiac GLP-1 receptors and LV function in patients with impaired and preserved LV function. The plasma GLP-1 level was significantly increased in patients with impaired LV function (5.7±1.9 pmol/L) as compared with those with preserved LV function (2.7±1.6 pmol/L). Plasma GLP-1 and plasma brain natriuretic peptide (BNP) levels were inversely correlated with the LV ejection fraction(EF), respectively. Plasma GLP-1 level positively correlated with plasma BNP level. Multivariate logistic regression analysis revealed that plasma GLP-1 level was an independent determinant of the impaired LV function, whereas plasma BNP level was not. Intensity of immunostaining for GLP-1 receptor protein was significantly enhanced in patients with impaired LV function compared with those with preserved LV function. The plasma GLP-1 level was increased in patients with impaired systolic LV function and inversely correlated with the LVEF. The expressions of GLP-1 receptors were enhanced in hearts with impaired LV function. These may suggest that endogenous GLP-1-GLP-1 receptor system serves as a compensatory mechanism for systolic LV dysfunction.
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