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ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #203175
Title: Cinnamon Extract Inhibits the Overproduction of Intestinal Apolipoprotein B-containing Lipoproteins in High-Fructose Fed Animals

Author
item QIN, BOLIN - PHYTOMEDICAL TECH, BC
item Anderson, Richard
item OSHIDA, YOSHIHARU - NAHOYA UNIVERSITY, JAPAN
item SATO, YUZO - NAHOYA UNIVERSITY, JAPAN

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/12/2007
Publication Date: 3/20/2007
Citation: Qin, B., Anderson, R.A., Oshida, Y., Sato, Y. 2007. Cinnamon Extract Inhibits the Overproduction of Intestinal Apolipoprotein B-containing Lipoproteins in High-Fructose Fed Animals. Federation of American Societies for Experimental Biology Conference. 21:839.8 A1075.

Interpretive Summary: n/a

Technical Abstract: We have reported previously that cinnamon extract (CE) prevents high-fructose (HF) feeding-induced decreases in insulin sensitivity and suggested that improvements of insulin sensitivity by CE were attributable, 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 hamster enterocytes. In an olive oil loading study, we found that acute CE (50mg/kg BW) oral treatment inhibited the serum triglyceride levels in HF fed rats but did not affect cholesterol and HDL levels. In a Triton-WR-1339 study, our results indicated that acute CE oral administration inhibited the overproduction of total apoB48 and chlyomicrons. In ex vivo studies, significant decreases were also observed in apoB48 secretion in 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.