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Purple‐fleshed potato, even after processing, prevents and reverses high‐fat diet elevated colonic‐mesenteric fatősystemic inflammation cascade in pig model (1045.47)
Author(s) -
Radhakrishnan Sridhar,
Kim Sung,
Reddivari Lavanya,
Vanamala Jairam
Publication year - 2014
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.28.1_supplement.1045.47
Subject(s) - inflammation , medicine , endocrinology , lipopolysaccharide , adipose tissue , systemic inflammation , oxidative stress , tumor necrosis factor alpha , chemistry
High‐fat diet (HFD) elevated colonic/adipose tissue inflammation strongly correlates with lipopolysaccharide (LPS) induced TLR‐4 activation. We have previously shown that purple‐fleshed potatoes (PP) suppress colonic/systemic oxidative stress markers in HFD consuming pigs. We hypothesized that PP, even after processing; suppress HFD induced colonic/mesenteric fat inflammation via suppression of LPS/TLR‐4 signalling compared to white‐fleshed potatoes (WP). We performed 2 studies ‐ a prevention study where 64 pigs consumed one of the 8 diets: Standard diet (SD), HFD and HFD supplemented with raw/baked/chips PP or WP (10% w/w) for 13 wk; and a reversal study where pigs (12 wk on HFD) consumed HFD containing 10/20% PP or WP chips for 5 wk (n=8). In the prevention study, all potato diets suppressed (P < 0.05) HFD elevated colonic/mesenteric fat expression of TLR‐4 and downstream NF‐κB and TNF‐α (qPCR), and serum IL‐1β (Immunoassay). In the reversal study, colonic/mesenteric fat expression of TLR‐4, NF‐κB and TNF‐α were consistently suppressed only in PP group (not WP) compared to HFD control (P < 0.05), suggesting that time of intervention is important. In addition, PP extracts suppressed LPS or TNF‐α induced NF‐κB activation in Caco‐2 cells compared to WP. Collectively, these results suggest that PP were more potent in reversing the HFD elevated colonic‐mesenteric fat‐systemic inflammatory cascade. Grant Funding Source : Supported by USDA‐NIFA NRI Grant 2009‐55200‐05197