The glycaemic outcomes of Cinnamon, a review of the experimental evidence and clinical trials

Arjuna B Medagama, Arjuna B Medagama

Abstract

Introduction: Cinnamon is currently marketed as a remedy for obesity, glucose intolerance, diabetes mellitus and dyslipidaemia. Integrative medicine is a new concept that combines conventional treatment with evidence-based complementary therapies.

Aim: The aim of this review is to critically evaluate the experimental evidence available for cinnamon in improving glycaemic targets in animal models and humans.

Results: Insulin receptor auto-phosphorlylation and de-phosphorylation, glucose transporter 4 (GLUT-4 ) receptor synthesis and translocation, modulation of hepatic glucose metabolism through changes in Pyruvate kinase (PK) and Phosphenol Pyruvate Carboxikinase (PEPCK), altering the expression of PPAR (γ) and inhibition of intestinal glucosidases are some of the mechanisms responsible for improving glycaemic control with cinnamon therapy. We reviewed 8 clinical trials that used Cinnamomum cassia in aqueous or powder form in doses ranging from 500 mg to 6 g per day for a duration lasting from 40 days to 4 months as well as 2 clinical trials that used cinnamon on treatment naïve patients with pre-diabetes. An improvement in glycaemic control was seen in patients who received Cinnamon as the sole therapy for diabetes, those with pre-diabetes (IFG or IGT) and in those with high pre-treatment HbA1c. In animal models, cinnamon reduced fasting and postprandial plasma glucose and HbA1c.

Conclusion: Cinnamon has the potential to be a useful add-on therapy in the discipline of integrative medicine in managing type 2 diabetes. At present the evidence is inconclusive and long-term trials aiming to establish the efficacy and safety of cinnamon is needed. However, high coumarin content of Cinnamomum cassia is a concern, but Cinnamomum zeylanicum with its low coumarin content would be a safer alternate.

Figures

Fig. 1
Fig. 1
Molecular mechanisms of Cinnamon by which it exerts hypoglycaemic activity. PK: Pyruvate Kinase, PEPCK: Phosphoenol Carboxy Kinase, PPAR-gamma: Peroxisome Proloferator Activated-Receptor gamma, WAT: White Adipose Tissue, ACO: Acyl-CoA Oxidase, GLUT-4: Glucose transporting protein 4, LPL: Lipoprotein lipase, CD36:Fatty Acid Transporter

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Source: PubMed

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