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Purple potato, even after processing, suppress oxidative stress and inflammatory markers in high‐fat diet consuming pigs
Author(s) -
Radhakrishnan Sridhar,
Reddivari Lavanya,
Smith Stephen B,
Kim Sung Woo,
Vanamala Jairam
Publication year - 2012
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.26.1_supplement.823.5
Subject(s) - oxidative stress , polyunsaturated fatty acid , fatty acid , malondialdehyde , adipose tissue , food science , obesity , inflammation , medicine , endocrinology , chemistry , biochemistry
Colored potatoes are becoming popular for their putative health benefits. Previously, we reported that purple potato (PP) chips suppressed the colonic inflammatory markers but did not alter feed intake/weight gain in the high‐fat diet (HFD) consuming pigs. However, no information exists if PP chips alter the systemic inflammatory markers. Elevated ratio of saturated fatty acids (SFA) to poly unsaturated fatty acids (PUFA) in adipose tissue of obese mice/humans leads to elevated inflammatory markers. We hypothesized that PP chips may alter mesenteric fat fatty acid profile and suppress systemic oxidative stress, and inflammatory markers compared to white potato (WP) chips in pigs consuming HFD. To test this hypothesis, obese pigs were provided with HFD containing 10/20 % PP/WP chips for 5 wks. Only PP diet (10%) suppressed oxidative stress markers (8‐isoprostane and malondialdehyde; ELISA, p < 0.05) compared to control and WP diet. Mesenteric fat free fatty acid analysis (GC) showed that PP and WP diet (10%, PP > WP) suppressed SFA and elevated PUFA compared to control. TNF‐α levels in serum were also suppressed (p < 0.05) by PP (10 and 20%) and WP (10%) diets compared to control. This suggests that PP, even after processing, might suppress oxidative stress/inflammatory markers in vivo via alterations in the fatty acid composition. Thus, consumption of colored potatoes may suppress chronic inflammation during obesity. Grant Funding Source : This work was supported by National Research Initiative Grant 2009‐55200‐05197 from the USDA National Institute for Food and Agriculture (2009–2012) and USDA AES (2010–2012) grant proposals.