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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 #210007
Title: Mechanisms of cinnamon extract-induced suppression of the overproduction of apolipoprotein B48-containing lipoproteins in insulin resistance

Author
item QIN, BOLIN - INTEGRITY NEUTRACEUTICALS
item Anderson, Richard

Submitted to: BARC Poster Day
Publication Type: Abstract Only
Publication Acceptance Date: 4/2/2007
Publication Date: 4/2/2007
Citation: Qin, B., Anderson, R.A. 2007. Mechanisms of cinnamon extract-induced suppression of the overproduction of apolipoprotein B48-containing lipoproteins in insulin resistance. BARC Poster Day.

Interpretive Summary:

Technical Abstract: Metabolic dyslipidemia is a common feature of insulin resistant states and is associated with aberrant metabolism of apoB-containing lipoprotein particles produced by not only the liver but also the small intestine. We have reported previously that an aqueous extract from cinnamon (CE) improves high-fructose (HF), feeding-induced, whole-body insulin resistance. In this study, we investigated whether intestinal apolipoprotein overproduction is inhibited by CE in rodent models of insulin resistance. Two hours following oral intake of cinnamon, 50 mg/kg body weight, CE inhibited total serum and triglyceride-rich lipoprotein (TRL)-apoB48 in fasted HF-fed rats. In a fat tolerance test, 200 ul of olive oil per rat, CE also inhibited the serum triglyceride levels in HF-fed rats, but did not affect cholesterol or HDL levels. CE also inhibited the TNF-alpha induced overproduction of TRL-apoB48 and VLDL-apoB48 in animals treated with Triton-WR-1339, an inhibitor of lipoprotein lipase. In ex vivo pulse-chase S35 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 in insulin resistance can be acutely inhibited by aqueous extracts from cinnamon in a process involving p38, ERK phosphorylation, and MTP expression. Supported by Integrity and USDA’S CRADA NO. 58-3K95-7-1184.