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United States Department of Agriculture

Agricultural Research Service

Title: Mechanisms of cinnamon extract-induced suppression of the intestinal overproduction of apolipoprotein B48-containing lipoproteins in insulin resistant high-fructose fed animals

Authors
item Qin, Bolin - INTEGRITY NEUTOCEUTICALS,
item Oshida, Yoshiharu - PHYSICAL FITNESS & SPORTS
item Sato, Yuzo - PHY.FIT.& SPORTS,JAPAN
item Adeli, Khostow - U OF TORONTO, ONTARIO
item Anderson, Richard

Research conducted cooperatively with:
item Integrity Neutraceuticals International

Submitted to: American Diabetes Association Meeting
Publication Type: Abstract Only
Publication Acceptance Date: October 5, 2007
Publication Date: June 22, 2007
Citation: Qin, B., Oshida, Y., Sato, Y., Adeli, K., Anderson, R.A. 2007. Mechanisms of cinnamon extract-induced suppression of the intestinal overproduction of apolipoprotein B48-containing lipoproteins in insulin resistant high-fructose fed animals. [abstract]. American Diabetes Association Meeting. 56:0911-P.

Technical Abstract: We have reported previously that cinnamon extract (CE) prevents high-fructose (HF) feeding-induced whole-body insulin resistance by enhancing insulin signaling in skeletal muscle. In this study, we investigated whether intestinal apolipoprotein overproduction is inhibited by CE in this insulin-resistant animal model. After a 2-hour acute CE oral treatment (50mg/kg body weight), CE significantly inhibited total serum and triglyceride-rich lipoprotein (TRL)-apoB48 in fasted HF-fed rats. In an olive oil-loading study, we also found that acute CE 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, acute CE oral administration inhibited the overproduction of total serum and TRL-apoB48. In ex vivo pulse-chase labeling studies, significant decreases were also observed in apoB48 secretion into media in freshly isolated enterocytes from HF-fed hamsters, together with increased apoB degradation. 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. CE also decreased the protein mass of intestinal microsomal triglyceride transfer protein (MTP) in CE treated HF-hamster enterocytes. In summary, these data suggest that the overproduction of apoB48 can be acutely inhibited by CE treatment in a process involving p38, ERK phosphorylation, and MTP expression.

Last Modified: 10/24/2014