Hostname: page-component-848d4c4894-pftt2 Total loading time: 0 Render date: 2024-05-31T04:44:01.427Z Has data issue: false hasContentIssue false

Curcumin and diabetes: a role for the vitamin D receptor?

Published online by Cambridge University Press:  01 November 2012

Barbara J. Boucher*
Affiliation:
Blizard Institute, Centre for Diabetes, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, LondonE12AT, UK email: bboucher@doctors.org.uk
Rights & Permissions [Opens in a new window]

Abstract

Type
Letter to the Editor
Copyright
Copyright © The Author 2012

A recent paper published in the British Journal Nutrition (Reference Gutierres, Pinhiero and Assis1) provides interesting data supporting the idea that curcumin can reduce metabolic and inflammatory problems induced by diabetes, including hyperglycaemia itself. Turmeric, the natural source of curcumin, is widely used as a colouring agent for sauces and manufactured foods as well as for cooking curries. The beneficial effects of curcumin on the liver, reported by the authors, will be especially important to pursue now that obesity and type 2 diabetes mellitus are increasing in prevalence and obesity comes to match malnutrition as a major health problem in many countries(Reference Wang, Chen and Shaikh2). In discussion of the possible reasons for the beneficial effects of curcumin, including increased insulin secretory responsiveness to glucose, increases in hepatic glucokinase activity and increased antioxidant-related protection of pancreatic islets(Reference Gutierres, Pinhiero and Assis1), the authors do not consider whether any of the non-insulin-related effects of curcumin could be accounted for by the vitamin D ligand-like actions of curcumin. Hormonal vitamin D (calcitriol) activates vitamin D receptors (VDR) and has mechanistic effects including increasing insulin secretory responsiveness to glucose, reducing abnormal islet renin–angiotensin activity, reducing inflammation and reducing abnormalities in several of the disorders used to define the metabolic syndrome(Reference Boucher3, Reference Cheng, Li and Boucher4). Thus, alternative activating ligands for the VDR such as curcumin can be expected to have similar effects(Reference Haussler, Whitfield and Kaneko5). The possibility that curcumin has some VDR-activating effect in the study of Gutierres et al. (Reference Gutierres, Pinhiero and Assis1) could be tested by determining whether or not serum parathyroid hormone (PTH) concentrations decrease with curcumin supplementation. A decrease in circulating PTH with curcumin treatment would support the suggestion that both insulin-related and non-insulin-related beneficial effects of curcumin could be mediated, at least in part, through VDR activation. This is because vitamin D supplementation in human hypovitaminosis D increases insulin secretory responses to glucose (in the absence of established type 2 diabetes mellitus) and may also reduce abnormally raised insulin resistance and suppress inflammation(Reference Hewison6).

References

1Gutierres, VO, Pinhiero, CM, Assis, RP, et al. (2012) Curcumin-supplemented yoghurt improves physiological and biochemical markers of experimental diabetes. Br J Nutr 108, 440448.Google Scholar
2Wang, Y, Chen, HJ, Shaikh, S, et al. (2009) Is obesity becoming a public health problem in India? Examine the shift from under- to over-nutrition problems over time. Obes Rev 10, 456474.Google Scholar
3Boucher, BJ (2012) Is vitamin D status relevant to metabolic syndrome? Dermatoendocrinol 4, 212224.Google Scholar
4Cheng, Q, Li, YC, Boucher, BJ, et al. (2011) A novel role for vitamin D: modulation of expression and function of the local renin–angiotensin system in mouse pancreatic islets. Diabetologia 54, 20772081.Google Scholar
5Haussler, MR, Whitfield, GK, Kaneko, I, et al. (2012) Molecular mechanisms of vitamin D action. Calcif Tissue Int (Epublication ahead of print version 11 July 2012).Google ScholarPubMed
6Hewison, M (2012) Vitamin D and immune function: autocrine, paracrine or endocrine? Scand J Clin Invest Suppl 243, 92102.Google Scholar