|Integrity Nutraceuticals International|
Submitted to: European Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 27, 2012
Publication Date: August 1, 2012
Citation: Qin, B., Dawson, H.D., Schoene, N.W., Polansky, M.M., Anderson, R.A. 2012. Cinnamon polyphenols regulate multiple metabolic pathways involved in intestinal lipid metabolism of primary small intestinal enterocytes. European Journal of Nutrition. 28:1172-79. Interpretive Summary: The small intestine is actively involved in the regulation of dietary lipid absorption, intracellular transport and metabolism, and is closely linked to fat and lipid metabolism. Cinnamon polyphenols have been shown to improve glucose, insulin, and lipid metabolism and improve inflammation in cell culture, animal and human studies. The aim of the study was to investigate the effects of an aqueous cinnamon extract on cells isolated from the small intestine of rats. The cinnamon extract inhibited the expression of genes involved with inflammation, and lipid metabolism but activated those involved in the improved function of insulin. These results demonstrate that compounds found in cinnamon may decrease inflammation and fats in the blood and also improve the function of insulin. These data should be of interest to scientists, medical personnel, and the lay public.
Technical Abstract: Increasing evidence suggests that dietary factors may affect the expression of multiple genes and signaling pathways including those that regulate intestinal lipoprotein metabolism. The small intestine is actively involved in the regulation of dietary lipid absorption, intracellular transport and metabolism, and is closely linked to systemic lipid metabolism. Cinnamon polyphenols have been shown to improve glucose, insulin, and lipid metabolism and reduce inflammation in cell culture, animal and human studies. However, little is known of the effects of an aqueous cinnamon extract (CE) on the regulation of genes and signaling pathways related to intestinal metabolism. The aim of the study was to investigate the effects of CE in the primary enterocytes of rats. Freshly isolated intestinal enterocytes were used to investigate gene expressions by quantitative RT-PCR and the protein and phosphorylation levels were evaluated by western blot and flow cytometry analyses. CE inhibited the mRNA expression of genes of the inflammatory cytokines, Il1ß, Il6, and Tnf-a, and induced the expression of the anti-inflammatory gene, Zfp36. CE also enhanced genes leading to increased insulin sensitivity including Ir, Irs1&2, Pi3k, and Akt1 and decreased Pten expression. CE inhibited genes associated with elevated cholesterol, triglycerides, and apolipoprotein B48 levels including Abcg5, Npc1l1, Scarb1, Cd36, Mttp, and Srebp1c, and facilitated Abca1 expression. CE also stimulated the phospho-p38 MAPK, JNK, and ERK expression determined by flow cytometry with no changes in the protein levels. These results demonstrate that CE leads to regulation of genes associated with insulin sensitivity, inflammation, and cholesterol/lipogenesis metabolism and the activity of MAPK signal pathway.