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The intestinal bioavailability of vaccenic acid and activation of peroxisome proliferator‐activated receptor‐α and ‐γ in a rodent model of dyslipidemia and the metabolic syndrome
Author(s) -
Wang Ye,
JacomeSosa Maria M.,
Ruth Megan R.,
Lu Yan,
Shen Jianheng,
Reaney Martin J.,
Scott Shan L.,
Dugan Michael E. R.,
Anderson Hope D.,
Field Catherine J.,
Proctor Spencer D.,
Vine Donna F.
Publication year - 2012
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201100517
Subject(s) - bioavailability , peroxisome proliferator activated receptor , endocrinology , triglyceride , chemistry , ppar agonist , medicine , receptor , peroxisome , peroxisome proliferator activated receptor delta , vaccenic acid , conjugated linoleic acid , fatty acid , pharmacology , biology , biochemistry , nuclear receptor , linoleic acid , cholesterol , gene , transcription factor
Scope Evidence suggests a neutral to beneficial role of certain trans fatty acids ( TFA ) from natural ruminant sources. Trans 11–18:1 (vaccenic acid, VA ), the most predominant ruminant TFA and a precursor to conjugated linoleic acid, has been shown to improve atherogenic dyslipidemia and symptoms of hepatic steatosis in animal models. The objective of this study was to assess the intestinal bioavailability of various VA sources including synthetic free fatty acid ( FFA ) and natural ruminant triglyceride forms, as well as the mechanistic pathways that mediate VA 's bioactivity. Methods and results VA acts as a partial agonist to both peroxisome proliferator‐activated receptors ( PPAR )‐α and PPAR ‐γ in vitro, with similar affinity compared to commonly known PPAR agonists. It was further confirmed that VA at 30 and 100 μM concentrations suppressed cardiomyocyte hypertrophy vitro in a PPAR ‐α‐ and PPAR ‐γ‐dependent manner. In vivo, feeding of VA (1%, w/w) resulted in increased m RNA and protein expression of PPAR ‐γ in the mucosa of JCR : LA ‐ cp rats, a model of the metabolic syndrome ( p < 0.01 and p < 0.05, respectively) compared to control. In addition, VA from a triglyceride source had greater intestinal bioavailability in vivo compared to VA provided in an FFA form ( p < 0.01). Conclusion The activation of PPAR ‐α‐ and PPAR ‐γ‐dependent pathways provides a mechanistic explanation of how VA improves blood lipids and related metabolic disorders during conditions of hyperlipidemia. This report also supports the consideration of differential reporting of industrially produced versus natural TFA on food nutrient labels.