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Endothelial dysfunction and outward remodeling in coronary and mesenteric arteries in response to high fat diet in mice
Author(s) -
Dunn Shan M.,
Hilgers Rob H. P.,
Das Kumuda C.
Publication year - 2016
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.30.1_supplement.1282.6
Subject(s) - endothelial dysfunction , myograph , medicine , endocrinology , pathophysiology , endothelium , mesenteric arteries , diabetes mellitus , population , coronary artery disease , artery , environmental health
It is well established that vascular endothelial dysfunction is an underlying mechanism in the pathophysiology of hypertension, atherosclerosis, diabetes and other cardiovascular diseases (CVD). Additionally, this cardiovascular pathophysiology is accentuated in aged population. We hypothesize that intake of high fat diet would exacerbate age‐related vascular endothelial dysfunction, promoting the onset and propagation of CVD. To test this hypothesis twelve‐week‐old male mice with C57BL6/J background were randomly divided into four groups and fed normal chow (NC) or HFS (42% fat) for a period of 3 or 12 months. We isolated the left coronary artery (LCA) and 2 nd ‐order mesenteric artery (MA) and mounted them in the wire‐ and pressure myograph. Both young and aged HFS mice had impaired glucose tolerance as well as an increase in cholesterol levels and weight gain compared to both groups of mice on NC. Aged HFS did have a significant increase in body weight (BW) when compared to young HFS. There was no difference in BW between young and aged mice on NC. Endothelium‐dependent ACh‐induced relaxing responses were blunted in MA and LCA from young HFS compared to young NC mice. Strikingly, this endothelial dysfunction was similar compared to aged NC mice. In addition, endothelial dysfunction in LCA and MA was worsened in aged HFS mice. MA from aged HFS mice developed outward hypertrophic remodeling compared to their younger counterparts and aged‐matched NC mice. These findings suggest that high fat diet in aged individuals can accelerate endothelial dysfunction and increase the risk of CVD. Support or Funding Information The work presented here is supported by NIH grant R01HL107885 and R01HL107885‐05S1