Submitted to: Journal of Nutritional Biochemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/15/2008
Publication Date: 11/6/2009
Citation: Qin, B., Polansky, M.M., Sato, Y., Adeli, K., Anderson, R.A. 2009. Cinnamon extract inhibits the postprandial overproduction of apolipoprotein B48-containing lipoproteins in fructose-fed animals. Journal of Nutritional Biochemistry. 20(11):901-908.
Interpretive Summary: For people with type 2 diabetes and related diseases, the problem is usually the fact that there is not too little insulin, but that the insulin present is not efficient; this condition is termed insulin resistance. Insulin resistance, which is often due to eating diets high in refined carbohydrates such as fructose and sucrose, affects the majority of the adult population in the U.S., and often leads to diabetes, cardiovascular diseases, inflammatory diseases, and even possibly Alzheimer’s disease. We have reported previously that consumption of cinnamon and specific cinnamon compounds prevents insulin resistance in experimental animals and humans. In this study, we examined the effects of compounds from cinnamon on insulin and fat metabolism. Consumption of diets high in refined carbohydrates by rats and hamsters led to elevated blood fats and also increased proteins that have negative effects on insulin and fat metabolism. Cinnamon compounds prevented these negative effects. We also investigated the molecular mechanisms of the effects of cinnamon on the expression of genes of the insulin signaling and fat metabolism pathways. Cinnamon improved both of these pathways. These data suggest that a cinnamon extract may improve blood and tissue fats by ameliorating intestinal insulin resistance and may be beneficial in the control of fat metabolism. These data are important to scientists, medical personnel, and the millions of people world-wide showing early signs of metabolic syndrome, or who have elevated blood sugar associated with insulin resistance.
Technical Abstract: We have reported previously that a cinnamon extract(CE)prevents fructose feeding-induced decreases in insulin sensitivity, and suggested that improvements of insulin sensitivity by CE were partly attributable to enhanced insulin signaling. In this study, we examined the effects of CE on postprandial apolipoprotein (apo) B-48 accumulation in fructose-fed rats, and the secretion of apoB48 in freshly isolated intestinal enterocytes of fructose-fed hamsters. Cinnamon extract (50mg/kg BW, given orally) inhibited serum triglyceride levels and the overproduction of total- and triglyceride-rich lipoprotein (TRL)-apoB48 in rats during an olive oil loading study. In addition, significant decreases were observed in apoB48 secretion into the media in enterocytes isolated from fructose-fed hamsters given CE. Quantitative real-time PCR was used to measure the effects of CE on the expression of genes of the insulin signaling pathway, including IRS1, IRS 2, and Akt1, and in lipid metabolism including MTP and SREBP1c in isolated, primary enterocytes from fructose-fed hamsters. The CE reduced expression of IR, IRS1, IRS2, and Akt1, and inhibited the over-expression of MTP and SREBP1c mRNA levels of enterocytes. The data suggest that the postprandial hypertriglyceridemia and the overproduction of apoB48 can be inhibited by CE through improved insulin sensitivity of intestinal enterocytes and regulation of MTP and SREBP1c. In addition, CE improves the postprandial overproduction of intestinal apoB48-containing lipoproteins by ameliorating intestinal insulin resistance and may be beneficial in the control of lipid metabolism.