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Physical activity prevents endothelial dysfunction induced by sedentary life style and high fat diet in murine coronary microcirculation
Author(s) -
Park Yoonjung,
Lee Sewon,
Booth Frank W,
Laye Matthew J,
Zhang Cuihua
Publication year - 2009
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.23.1_supplement.952.4
Subject(s) - medicine , endocrinology , insulin resistance , leptin , endothelial dysfunction , vasodilation , endothelium , obesity , insulin
Sedentary life style and high fat diet increase a risk of diabetes and cardiovascular diseases, but physical activity counteracts high fat diet‐induced vascular dysfunction. Our goal was to investigate the mechanisms by which physical activity prevents endothelial dysfunction caused by high fat diet. Female mice (C57BL/6) were fed either control low‐fat diet (LF; 15% fat) or high‐fat diet (HF; 45% fat) for 10 weeks. HF mice were randomly assigned to either a sedentary group or a group given access to a voluntary running wheel (HF‐Run). HF sedentary group was divided to HF‐Lean (HF‐LN; body weight<28g) and HF‐Obese (HF‐OB; body weight>28g) group. Endothelium‐dependent dilation (isolated coronary arterioles) to acetylcholine and to flow were impaired in HF‐OB mice, but were greater in HF‐Run and HF‐LN mice compared to HF‐OB mice. Leptin‐mediated vasodilation was higher in HF‐LN compared to HF‐OB. Compared to LF, HF‐LN, and HF‐Run mice, leptin levels and insulin resistance were higher in HF‐OB mice. These results suggest that the leptin and insulin resistance caused by high fat diet were reversed by physical activity. Also physical activity prevented high fat‐induced endothelial dysfunction, which may be mediated and improved leptin and insulin sensitivity.