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Dietary isoflavone intake modulates evoked responses to cardiometabolic stimuli in healthy volunteers
Author(s) -
Ferguson Jane Francisca,
TutejaStevens Sony,
Shah Rhia Y,
Patel Parth N,
Rader Daniel J,
Reilly Muredach P
Publication year - 2013
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.27.1_supplement.lb399
Subject(s) - isoflavones , endocrinology , medicine , phytoestrogens , tumor necrosis factor alpha , inflammation , estrogen
Isoflavones, found in high concentrations in soy‐derived foods, function as phytoestrogens, have antioxidant and anti‐inflammatory activity, inhibit protein‐tyrosine kinase activity, and are thought to be atheroprotective. We hypothesized that habitual isoflavone intake modulates response to evoked endotoxemia and oral fat load. In the Genetics of Evoked Responses to Niacin and Endotoxemia (GENE) Study, we administered low dose endotoxin (LPS 1 ng/kg) to induce inflammation in young, healthy volunteers (N=215, 50% female) and administered a separate oral fat tolerance test (OFTT). Data were analyzed using linear regression models adjusted for race, gender, age and BMI. Dietary isoflavone intake was a significant predictor of plasma tumor necrosis factor alpha (TNFα) and interleukin 6 (IL‐6) post LPS. High (>;1.5mg/day, N=64) vs low (<1.5mg/day, N=151) isoflavone consumers had higher peak TNFα (64 vs 45 pg/ml, P=0.015) and peak IL‐6 (210 vs 160 pg/ml, P=0.06). Further, the high isoflavone group had significantly higher β‐hydroxybutyrate levels post‐OFTT (442 vs 332 μmol/L, 2 hours post fat load, P=0.02). Habitual isoflavone consumption may modulate disease development through effects on inflammatory and metabolic responses in humans. For investigating nutritional effects on disease development, measuring evoked phenotypes may be more informative than describing resting characteristics. The GENE Study was supported by NIH Grant UL1TR3 as well as a NIH‐NHLBI SCCOR Project grant (P50‐HL‐083799) to MPR. JFF is supported by an AHA postdoctoral fellowship grant (12POST11840017).

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