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A diet rich In saturated fat impairs endothelium dependent relaxation (EDR) In Guinea Pig (GP)
Author(s) -
Edirisinghe Indika,
Siva Brahmesh,
Randolph Jody,
Steinberg Francene,
Skepper Jeremy,
Kappagoda Tissa
Publication year - 2006
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.20.4.a287-a
Subject(s) - chemistry , enos , medicine , corn oil , endocrinology , coconut oil , receptor , food science , biochemistry , biology , nitric oxide synthase , enzyme
We tested the hypothesis that a diet enriched with saturated coconut fat (CF) impairs EDR. 3 groups (n=6) of male 10 wk old GP (Hartley) were fed isocaloric diets containing (w/w) either 5% CF (Group1), 5% CF+corn oil (1:1) (Group2) or 5% corn oil (Group3). They were sacrificed after 12 wk and plasma lipids were estimated. Aorta was harvested for measuring EDR. EDR was measured in conventional organ baths containing Krebs buffer after pre‐contraction with noradrenaline (10 −5 M). EDR evoked by acetylcholine (Ac), bradykinin (Br), Ca ionophore (Cai) and grape seed extract (GSE) were measured. Aorta from one GP in each group was pressure fixed for immunohistochemistry (IHC).EDR to Br was lowest in the 5% CF group. EDR to Cai and GSE were unaffected in all groups. IHC confirmed the presence of eNOS in all groups. EDR to Ac was absent in all groups. It was also absent in age matched GP’s fed a diet containing 0.5% fat, but present (20 %) in 10 wk old GP’s. The loss of EDR to Br is probably due to a change in receptors induced by the CF diet and not due to down‐regulation of e‐NOS or its ability to produce NO. Loss of EDR to Ac should not be viewed as a marker for bioavailability of e‐NOS in the GP. The absence of EDR to Ac is probably due to an age related loss of functional receptors. Supported ‐ Polyphenolics Inc.