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Cinnamon extract inhibits the overproduction of intestinal apolipoprotein B‐containing lipoproteins in high‐ fructose fed animals‐Evidence from in vivo and ex vivo studies
Author(s) -
Qin Bolin,
Anderson Richard A,
Oshida Yoshiharu,
Sato Yuzo
Publication year - 2007
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.21.6.a1075-c
Subject(s) - medicine , hamster , endocrinology , overproduction , chylomicron , apolipoprotein b , ex vivo , in vivo , triglyceride , chemistry , insulin resistance , lipoprotein , cholesterol , biology , biochemistry , insulin , in vitro , very low density lipoprotein , microbiology and biotechnology , enzyme
We have reported previously that cinnamon extract (CE) prevents high‐fructose (HF) feeding‐induced insulin resistance due, at least in part, to enhanced insulin signaling in skeletal muscle. In this study, we examined the effects of CE on intestinal apolipoprotein (apo) B production in HF‐fed rats, and in hamster enterocytes. In an olive oil‐loading study, we found that acute CE (50mg/kg body weight) oral treatment inhibited the serum triglyceride levels in HF‐fed rats, but did not affect cholesterol or HDL levels. In a Triton‐WR‐1339 study, our results indicated that acute CE oral administration inhibited the overproduction of total apoB48 and chylomicrons. In ex vivo studies, significant decreases were also observed in apoB48 secretion into media in enterocytes isolated from HF‐fed hamsters, together with increased apoB degradation. Our data also demonstrated that CE decreased the phosphorylation of p38 and ERK in normal hamster primary enterocytes, and increased the impaired phosphorylation of p38 and ERK in HF‐fed hamster enterocytes. In summary, these data suggest that the overproduction of apoB48 in Triton‐WR‐1339‐treated rats and hamster enterocytes can be acutely inhibited by CE in a process involving enhanced apoB48 degradation. This appears to lead to a significant amelioration of intestinal apoB overproduction observed in HF‐fed animals.