人間における循環粘着分子:高血糖症と高インスリン血症の役割
R Marfella1, K Esposito, R Giunta
1Department of Geriatrics, Second University of Naples, Naples, Italy.
Circulation
|May 16, 2000
まとめ
急性高血糖症は,健康な個体において,溶性細胞間粘着分子-1 (sICAM-1) を上昇させます. 2型糖尿病では,インスリンまたはL-アルギニンが上昇したsICAM-1レベルを正常化する.
科学分野:
- エンドクリノロジー エンドクリノロジー
- 血管生物学 血管生物学
- メタボリック障害 メタボリック障害
背景:
- 溶性細胞間粘着分子-1 (sICAM-1) と血管粘着分子-1 (sVCAM-1) の循環レベルは,血管炎症に関与しています.
- これらの粘着分子の調節におけるグルコースとインスリンの役割は,特に2型糖尿病では完全に理解されていません.
研究 の 目的:
- グルコースとインスリンがsICAM-1およびsVCAM-1レベルに与える影響を調査する.
- 正常な被験者と2型糖尿病患者におけるこれらの効果を比較する.
主な方法:
- ハイパーグリセミッククランプの研究は,正常な被験者と2型糖尿病患者で実施されました.
- オクトレオチドは,クランプ中にインスリン放出を抑制するために使用されました.
- 糖尿病患者の人工臓またはL-アルギニンサプリメントを使用してユーグリセミアを達成しました.
主要な成果:
- 急性高血糖症は,正常な被験者のsICAM-1レベルを著しく上昇させた.
- 糖尿病患者は対照群と比較して,ベースラインより高いsICAM-1濃度を示した.
- インスリン阻害は,sICAM-1の上昇を悪化させ,インスリンまたはL-アルギニンは,糖尿病患者のsICAM-1を正常化する.
結論:
- 急性高血糖症は,循環中のsICAM-1を増加させる刺激である.
- インスリンとL-アルギニンは,2型糖尿病におけるsICAM-1濃度の上昇を正常化する役割を果たします.
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