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High fat‐diet induced obesity does not necessarily promote vascular remodeling/fibrosis in rats
Author(s) -
Fernandes Roxanne,
CarterTaylor Evan,
Galligan James,
Xu Hui
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.961.1
Subject(s) - medicine , endocrinology , fibrosis , inflammation , mesenteric arteries , vascular smooth muscle , adipose tissue , artery , smooth muscle
Inflammation and hyperglycemia are responsible for obesity associated vascular remodeling/fibrosis. Our lab has previously observed that high fat (HF) diet‐induced obesity and hyperglycemia promote vascular remodeling/fibrosis, but HF diet does not necessarily promote hypertension in male mice. However, it is unclear if vascular remodeling/fibrosis and inflammation are unique changes in all HF diet‐induced obese rodent models. In current studies, we compared the blood pressure, vascular and tissue histological structures of heart, mesentery, and kidney in male and female Sprague Dawley rats fed with HF (60 kcal% fat) or control (10 kcal% fat) diet up to 20 or 48 weeks. Vascular responsibilities to norepinephrine and wall thickness/distensibility were evaluated in pressurized mesenteric arteries (MA) and veins (MV) in vitro . The plasma levels of TNA‐α, monocyte chemoattractant protein‐1 (MCP‐1), insulin, glucose and leptin were also evaluated in these rats. HF fed female (20 weeks) and male (48 weeks) rats were obese and hyperleptinemia, but normotensive and with unchanged vascular contractility. These rats did not exhibit vascular remodeling/fibrosis, hyperglycemia, and systemic inflammation, when compared with control diet fed rats. After 48 weeks of exposure to HF diet, female rats were obese, hyperleptinemia, hypertensive and with reduced vascular reactivity to norepinephrine, however, these rats did not exhibit vascular remodeling/fibrosis, hyperglycemia, or systemic inflammation either. Our findings suggested that obesity is not the determinant in the development of vascular fibrosis/remodeling. HF diet induced hyperglycemia and tissue inflammation may be the predominant mediators in obesity associated vascular remodeling/fibrosis. Support or Funding Information Supported by Undergraduate Research in Biomedical Sciences Program (NIH grant HL103156, for Dr. Ewart to support Carter‐Taylor) and NIH grant 2P01HL070687 (For Drs Galligan and Xu)