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The t10c12 conjugated linoleic acid (CLA) isomer prevents the development of obesity‐related hypertension by increasing plasma adiponectin and activating endothelial nitric oxide synthase (eNOS) in fa/fa Zucker rats
Author(s) -
DeClercq Vanessa,
Taylor Carla G.,
Zahradka Peter
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.543.1
Subject(s) - enos , medicine , adiponectin , endocrinology , adipose tissue , chemistry , white adipose tissue , conjugated linoleic acid , nitric oxide , obesity , linoleic acid , nitric oxide synthase , insulin resistance , biology , biochemistry , fatty acid
Obesity‐related hypertension may be due to increased activation of the adipose tissue renin‐angiotensin system (RAS) and/or reduced eNOS activity. CLA, a mixture of positional and geometric isomers of linoleic acid, has been shown to reduce blood pressure (BP) in obese insulin‐resistant rats. We investigated whether CLA isomers target RAS or eNOS by exploring expression of molecules related to BP regulation in obesity. Fa/fa Zucker rats were randomly assigned to 1 of 4 groups: (1) control (2) c9t11‐CLA (3) t10c12‐CLA (4) captopril. Systolic BP significantly increased in untreated obese rats during the 8‐week study. This increase of systolic BP was attenuated in the t10c12‐CLA isomer or captopril groups. Angiotensinogen, eNOS and adiponectin expression were examined by Western blot analysis and plasma adiponectin by ELISA. The t10c12‐CLA isomer increased plasma adiponectin levels however, no differences were seen in protein expression in white adipose tissue. Feeding the t10c12‐CLA isomer significantly increased phospho‐eNOS expression in white adipose tissue and the aorta. No changes were observed in angiotensinogen expression in white adipose tissue or aorta. In conclusion, the t10c12‐CLA isomer attenuates the development of obesity‐related hypertension, at least in part, by elevating circulating adiponectin and activating eNOS. Grant Funding Source NSERC