|Qin, Bolin -|
|Integrity Nutraceuticals International|
Submitted to: Hormone and Metabolic Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 16, 2009
Publication Date: March 10, 2010
Citation: Qin, B., Polansky, M.M., Anderson, R.A. 2010. Cinnamon extract regulates plasma levels of adipose-derived factors and expression of multiple genes related to carbohydrate metabolism and lipogenesis in adipose tissue of fructose-fed rats. Hormone and Metabolic Research. 42:187-193. Interpretive Summary: Fat tissue has been considered as only a passive organ for fat storage and not directly involved in the control of risk factors associated with the causes of type 2 diabetes and cardiovascular diseases. However, increasing evidence suggests that fat tissue is an active endocrine organ, releasing hormones and growth factors that are collectively called adipokines and are involved in sugar and fat metabolism throughout the body. In the present study, we examined the effects of a cinnamon extract on several biomarkers including plasma levels of adipose-derived adipokines, and the potential molecular mechanisms of a cinnamon extract to decrease risk factors of diabetes and cardiovascular diseases. In rats fed a high-fructose diet to induce insulin resistance, supplementation with a cinnamon extract reduced blood glucose, plasma insulin, triglycerides, total cholesterol, and several fatty components of the blood that have negative effects on the onset of type 2 diabetes and cardiovascular diseases. These results suggest that a cinnamon extract effectively normalizes circulating levels of adipokines by the regulation of multiple genes involved in insulin sensitivity and fat synthesis. This study will be of benefit to scientists working on the mechanisms involved in the onset of diseases related to the metabolic syndrome and potentially to people at risk for type 2 diabetes and(or) cardiovascular diseases.
Technical Abstract: We reported previously that a dietary cinnamon extract (CE) improves systemic insulin sensitivity and dyslipidemia by enhancing insulin signaling. In the present study, we examined the effects of CE on several biomarkers including plasma levels of adipose-derived adipokines, and the potential molecular mechanisms of CE in epididymal adipose tissue. In rats fed a high-fructose diet (HFD) to induce insulin resistance, supplementation with CE (Cinnulin PF, 50 mg/kg BW daily) for 8 wk reduced blood glucose, plasma insulin, triglycerides, total cholesterol, chylomicron-apoB48, VLDL-apoB100, and soluble CD36. CE also inhibited plasma retinol binding protein 4 (RBP4) and fatty acid binding protein 4 (FABP4) levels. CE-induced increases in plasma adiponectin were not significant. In the epididymal adipose tissue, there were increases the in insulin receptor (Ir) and Ir substrate 2 (Irs2) mRNA but CE-induced increases in mRNA expression of Irs1, phosphoinositide-3-kinase (Pi3k), v-akt murine thymoma viral oncogene homolog 1 (Akt1), glucose transporters 1 & 4 (Glut1, Glut4), and glycogen synthase 1 (Gys1) expression and decreased trends in mRNA expression of glycogen synthase kinase 3ß (Gsk3ß) were not statistically significant. CE also enhanced the mRNA levels of adipoQ, and inhibited sterol regulatory element binding protein-1c (Srebp1c) mRNA levels. mRNA and protein levels of fatty acid synthase (FAS) and FABP4 were inhibited by CE and RBP4 and CD36 protein levels were also decreased by CE. These results suggest that CE effectively ameliorates circulating levels of adipokines partially mediated via regulation of the expression of multiple genes involved in insulin sensitivity and lipogenesis in adipose tissue.