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TNF‐á inhibits stimulation of apolipoprotein A‐IV expression induced by linoleic acid (LA) in Caco2 cells
Author(s) -
Li Xiaoming,
Xu Min,
Liu Min,
Li Yong,
Tso Patrick
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.lb767
Subject(s) - endocrinology , medicine , apolipoprotein b , stimulation , tumor necrosis factor alpha , proinflammatory cytokine , obesity , inflammation , chemistry , biology , cholesterol
Background Chronic feeding of a HF diet significantly reduces intestinal as well as hypothalamic apolipoprotein A‐IV (apoA‐IV) gene expression by fat feeding. Since apoA‐IV suppresses food intake, this blunting of gut & hypothalamic responses to fat feeding may contribute to diet‐induced obesity. It is well established that the circulating pro‐inflammatory cytokines are increased by HF feeding. Aim The following study was conducted to determine if pro‐inflammatory cytokines are involved in blunting the apoA‐IV responses to fat feeding. Results & Discussions LA, an important dietary fatty acid, was used to stimulate apoA‐IV expression in human intestinal Caco2 cells. Cells were pre‐treated with or without human recombinant TNF‐á, IL‐6 or both before the addition of LA to stimulate apoA‐IV expression. ApoA‐IV mRNA levels were measured by real‐time RT‐PCR. LA stimulated apoA‐IV expression markedly in a dose and time dependent manner. Pre‐treatment with the cytokines for 48 or 72 h, especially with TNF‐á, significantly reduced the mRNA of apoA‐IV induced by LA. Conclusions We conclude that pro‐inflammatory cytokines, especially TNF‐á, are responsible for blunting of apoA‐IV response to fat feeding. Because of apoA‐IV's role in satiety, this interaction between circulating pro‐inflammatory cytokines and apoA‐IV may contribute to diet‐induced obesity. Supported by NIH DK 59630, DK 92138, and DK 76928.