Prospective Nutraceutical Effects of Cinnamon Derivatives Against Insulin Resistance in Type II Diabetes Mellitus-Evidence From the Literature

Abstract

Apart from advances in pharmaceutical antidiabetic agents, efforts are being made toward hypoglycemic agents derived from natural sources. Cinnamon has been reported to have significant benefits for human health, particularly as an anti-inflammatory, antidiabetic, and anti-hypertriglyceridemic agent. The phytochemicals in cinnamon can be extracted from different parts of plant by distillation and solvent extraction. These chemicals help in decreasing insulin resistance and can act against hyperglycemia and dyslipidemia, inflammation and oxidative stress, obesity, overweight, and abnormal glycation of proteins. Cinnamon has shown to improve all of these conditions in in vitro, animal, and/or human studies. However, the mechanism of action of active ingredients found in cinnamon remains unclear. The current review presents the outstanding ability of cinnamon derivatives to control diabetes by various pathways modulating insulin release and insulin receptor signaling. It was also found that the type and dosage of cinnamon as well as subject characteristics including drug interactions are likely to affect the response to cinnamon. Future research directions based on this review include the synergistic usage of various cinnamon derivatives in managing and/or preventing diabetes and possible other relevant chronic diseases.

Keywords: cinnamon; diabetes mellitus; fasting blood glucose; hyperglycemia.

Figure 1.

Insulin signaling pathway. Protein-tyrosine phosphatase 1B; PTP1B, insulin receptor substrate; IRS, ROCK, PIP, Rho-kinase; PTEN, phosphatase, phosphatidylinositol phosphate; and tension homologue deleted on chromosome 10; Pleckstrin homology domain; PDK, PH domain, GβL, phosphoinositide-dependent protein kinase; G-protein beta subunit like; mTOR, substrate; PKCλ/ζ, protein kinase C λ and mammalian target of rapamycin; AS160, 160 kDa Akt ζ; GLUT4, glucose transporter 4.

Figure 2.

Target treatment for T2DM (DPP – 4i, dipeptidyl peptide – 4 inhibitor; TZDs, thiazolidinediones; SGLT-2i, sodium–glucose co-transporter 2 inhibitor; GLP-1RA, glucagon-like peptide – 1 receptor agonist).

Figure 3.

PROMPT guidelines for managing T2DM.

Figure 4.

A model of actions of cinnamon polyphenols (CPs) in the insulin signal transduction pathway leading to beneficial effects in subjects with glucose intolerance or type 2 diabetes. IRS, insulin receptor substrate; PI3K, 1-phosphatidylinositol 3-kinase; PIP2, phosphatidylinositol 4,5-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PTP-1, protein-tyrosine phosphatase-1; PDK1, phosphatidylinositol-dependent protein kinase 1; FAT, fat; G-6-P, glucose 6-phosphate; PKB, protein kinase B; UDPG, uridine diphosphoglucose; GM-CSF, granulocyte–macrophage colony-stimulating factor; Cox2, cyclooxygenase-2; VEGF, vascular endothelial growth factor; –, negative effect; +, positive effect.