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Regional Variation in Arterial Stiffening and Dysfunction in Western Diet‐Induced Obesity
Author(s) -
Bender Shawn,
CastorenaGonzalez Jorge,
Garro Mona,
ReyesAldasoro Constantino,
Sowers James,
DeMarco Vincent,
MartinezLemus Luis
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb606
Subject(s) - arterial stiffness , pulse wave velocity , medicine , cardiology , femoral artery , aorta , ex vivo , artery , in vivo , endocrinology , anatomy , blood pressure , biology , microbiology and biotechnology
Central vascular stiffening, determined in vivo via pulse wave velocity (PWV), independently predicts cardiovascular event risk and is accelerated in obesity. Little is known regarding potential regional variations in arterial stiffening in obesity. We assessed aortic and femoral PWV with ex vivo analyses of femoral and coronary structure/function in a mouse model of western diet (WD; high‐fat/high‐sugar)‐induced obesity. WD increased aortic and femoral PWV. Ex vivo femoral artery analysis revealed a leftward shift in the strain‐stress relationship, increased modulus of elasticity, and decreased compliance indicative of increased stiffness following WD. Confocal and multiphoton fluorescence microscopy revealed that increased femoral stiffness involved decreased elastin/collagen ratio in WD. Analysis of the femoral internal elastic lamina (IEL) revealed reduced number and size of fenestrae with WD. Coronary artery stiffness/structure was unchanged by WD. Functionally, femoral, not coronary, arteries exhibited endothelial dysfunction while coronary, not femoral, arteries exhibited increased vasoconstrictor responsiveness. Overall, our data highlight important regional variations in arterial stiffening/dysfunction and highlight IEL fenestrae remodeling as a potential contributor to femoral artery stiffening in obesity.