Location: Diet, Genomics and Immunology LaboratoryTitle: Cinnamon increases liver glycogen in an animal model of insulin resistance Author
Submitted to: Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/22/2011
Publication Date: 5/6/2011
Citation: Couturier, K., Qin, B., Batandier, C., Awada, M., Hininger, I., Canini, F., Leverve, X., Roussel, A., Anderson, R.A. 2011. Cinnamon increases liver glycogen in an animal model of insulin resistance. Metabolism. 60(11):1590-7. Interpretive Summary: Cinnamon and water extracts of cinnamon improve insulin sensitivity and thus glucose utilization in cell culture, animal, and human studies. The objectives of this study were to determine the effects of cinnamon on formation of glycogen (a storage form of carbohydrate found in muscle and in the liver), on genes that control its formation, and protein levels in muscle and liver tissue. Liver and muscle glycogen are the major storage forms of energy. Rats fed a high fat/high fructose diet were used to evaluate the effects. This diet causes insulin resistance and elevated blood glucose levels in rats and thus is a useful animal model of human response. Four groups of rats were fed for 12 weeks with (i) the high fat/high fructose diet to induce insulin resistance, (ii) same diet containing 20 g cinnamon/kg of diet, (iii) a control diet, and (iv) a control diet containing 20 g cinnamon/kg of diet. The high fat/high fructose diet caused a significant decline in insulin function that was reversed by consuming cinnamon. Cinnamon added to the high fat/high fructose diet led to highly significant improvements in insulin function and increases of glycogen levels in the liver but not in muscle. Cinnamon also counteracted decreases in the insulin signalling proteins normally induced by the high fat/high fructose diet. Improvements due to cinnamon in animals consuming the control diet (normal fat and no fructose) were not significant. In summary, these data suggest that, in rats made insulin resistant due to feeding a high fat/high fructose diet, cinnamon improves insulin sensitivity and increases the content of liver glycogen by regulating insulin signalling and glycogen synthesis. These data should be of interest to scientists, medical personnel, and the lay public.
Technical Abstract: Cinnamon, and aqueous polyphenol extracts of cinnamon, improve insulin sensitivity in vitro, and in animal and human studies. Given the relationship between the glucose/insulin system and glycogen metabolism, the objective of this study was to determine the effects of cinnamon on glycogen synthesis, related gene expression and protein levels in the muscle and liver using an animal model of insulin resistance, the high fat/high fructose diet (HF/HFr) fed rat. Four groups of 22 male Wistar rats were fed for 12 weeks with (i) (HF/HFr) diet to induce insulin resistance, (ii) HF/HFr diet containing 20 g cinnamon/kg of diet, (iii) a control diet, and (iv) the control diet containing 20 g cinnamon/kg of diet. A significant decrease of the glucose infusion rate, assessed by hyperinsulinemic euglycemic clamps, was measured in rats fed the HF/HFr diet. Addition of cinnamon to the HF/HFr diet reversed the glucose infusion rates to those of the control rats. In liver, cinnamon added to the HF/HFr diet led to highly significant increases of glycogen levels. Increases in muscle glycogen due to cinnamon were not significant. In the liver, cinnamon also counteracted the decreases of Ir, Irs1, Irs2, Glut1, Glut2, and glycogen synthase 1 gene expression induced by the HF/HFr diet. In muscle, the decreased Ir, Irs1, Irs2, Glut1, Glut4 and glycogen synthase 1 induced by HF/HFr diet were also reversed by cinnamon. In addition, the over expression of Gsk3b mRNA levels and protein observed in the muscle of HF/HFr fed rats were decreased by animals consuming cinnamon. In summary, these data suggest that, in insulin resistant HF/HFr fed rats, cinnamon improves insulin sensitivity and enhances liver glycogen via regulating insulin signalling and glycogen synthesis.