Insulin Resistance and Endothelial Dysfunction: A Mutual Relationship in Cardiometabolic Risk

被引:46
作者
Del Turco, Serena [1 ]
Gaggini, Melania [1 ,2 ]
Daniele, Giuseppe [2 ,3 ]
Basta, Giuseppina [1 ]
Folli, Franco [3 ]
Sicari, Rosa [1 ]
Gastaldelli, Amalia [1 ,3 ]
机构
[1] CNR, Inst Clin Physiol, Pisa, Italy
[2] Univ Pisa, Pisa, Italy
[3] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA
关键词
Endothelial dysfunction; insulin resistance; insulin signaling pathways; cardiometabolic risk; FREE FATTY-ACID; GLUCAGON-LIKE PEPTIDE-1; PROTEIN-KINASE-C; ACTIVATOR INHIBITOR TYPE-1; GLYCATION END-PRODUCTS; BODY-MASS INDEX; SKELETAL-MUSCLE; NITRIC-OXIDE; METABOLIC SYNDROME; MICROVASCULAR RECRUITMENT;
D O I
10.2174/1381612811319130010
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cardiometabolic risk comprises a cluster of traditional and emerging factors that are good indicators of a patient's overall risk for type 2 diabetes and cardiovascular disease. The insulin resistance, a key feature common to obesity and type 2 diabetes, is associated with impaired vascular response and contributes to increased cardiovascular risk. Abnormal vascular insulin signalling induces endothelial dysfunction, the initial step of atherosclerotic process, characterized by attenuated nitric oxide-mediated vasodilatation and atherogenic response. Insulin resistance and endothelial dysfunction are two pathological conditions that can co-exist, even if their cause-effect relationship is not yet clarified. Multiple signaling pathways shared by insulin resistance and endothelial dysfunction include hyperinsulinemia, glucotoxicity, lipotoxicity, and inflammation. These mechanisms selectively impair PI3K-dependent insulin in vascular endothelium harming endothelial balance and strengthening the evidence of the close association between metabolic and cardiovascular disease. The present review analyzes the close relationship between endothelial dysfunction and insulin resistance and explores the common mechanisms, with clinical considerations and pharmacological strategies.
引用
收藏
页码:2420 / 2431
页数:12
相关论文
共 161 条
[11]   MECHANISM OF INSULIN RESISTANCE IN INSULIN-DEPENDENT DIABETES-MELLITUS - A MAJOR ROLE FOR REDUCED SKELETAL-MUSCLE BLOOD-FLOW [J].
BARON, AD ;
LAAKSO, M ;
BRECHTEL, G ;
EDELMAN, SV .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 73 (03) :637-643
[12]  
Baron Alain D., 1996, American Journal of Physiology, V271, pE1067
[13]   Insulin regulates its own delivery to skeletal muscle by feed-forward actions on the vasculature [J].
Barrett, Eugene J. ;
Wang, Hong ;
Upchurch, Charles T. ;
Liu, Zhenqi .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2011, 301 (02) :E252-E263
[14]   Advanced glycation end products activate endothelium through signal-transduction receptor RAGE - A mechanism for amplification of inflammatory responses [J].
Basta, G ;
Lazzerini, G ;
Massaro, M ;
Simoncini, T ;
Tanganelli, P ;
Fu, CF ;
Kislinger, T ;
Stern, DM ;
Schmidt, AM ;
De Caterina, R .
CIRCULATION, 2002, 105 (07) :816-822
[15]   Dose-response effect of elevated plasma free fatty acid on insulin signaling [J].
Belfort, R ;
Mandarino, L ;
Kashyap, S ;
Wirfel, K ;
Pratipanawatr, T ;
Berria, R ;
DeFronzo, RA ;
Cusi, K .
DIABETES, 2005, 54 (06) :1640-1648
[16]   Accurate assessment of β-cell function -: The hyperbolic correction [J].
Bergman, RN ;
Ader, M ;
Huecking, K ;
Van Citters, G .
DIABETES, 2002, 51 :S212-S220
[17]   Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation [J].
Bjornholm, M ;
Kawano, Y ;
Lehtihet, M ;
Zierath, JR .
DIABETES, 1997, 46 (03) :524-527
[18]   Relationships between human serum resistin, inflammatory markers and insulin resistance [J].
Bo, S ;
Gambino, R ;
Pagani, A ;
Guidi, S ;
Gentile, L ;
Cassader, M ;
Pagano, GF .
INTERNATIONAL JOURNAL OF OBESITY, 2005, 29 (11) :1315-1320
[19]   Endothelial lipase: A modulator of lipoprotein metabolism upregulated by inflammation [J].
Broedl, UC ;
Jin, WJ ;
Rader, DJ .
TRENDS IN CARDIOVASCULAR MEDICINE, 2004, 14 (05) :202-206
[20]   Suppressor of cytokine signaling-3 provides a novel interface in the cross-talk between angiotensin II and insulin signaling systems [J].
Calegari, VC ;
Alves, M ;
Picardi, PK ;
Inoue, RY ;
Franchini, KG ;
Saad, MJA ;
Velloso, LA .
ENDOCRINOLOGY, 2005, 146 (02) :579-588