Indian Journal of Human Genetics
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Year : 2012  |  Volume : 18  |  Issue : 3  |  Page : 274-275
 

Vitamin D receptor and type 2 diabetes mellitus: Growing therapeutic opportunities


1 Department of Radiation Oncology, James Cancer Center, The Ohio State University, Columbus, OH 43210, USA
2 Center for Childhood Cancer, Nationwide Children's Hospital, Columbus, Ohio 43205, USA

Date of Web Publication4-Mar-2013

Correspondence Address:
Hemant K Bid
Center for Childhood Cancer, The Research Institute, Nationwide Children’s Hospital, 700 Children’s Drive, Columbus, OH 43205
USA
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DOI: 10.4103/0971-6866.107975

PMID: 23716932

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How to cite this article:
Manchanda PK, Bid HK. Vitamin D receptor and type 2 diabetes mellitus: Growing therapeutic opportunities. Indian J Hum Genet 2012;18:274-5

How to cite this URL:
Manchanda PK, Bid HK. Vitamin D receptor and type 2 diabetes mellitus: Growing therapeutic opportunities. Indian J Hum Genet [serial online] 2012 [cited 2014 Sep 17];18:274-5. Available from: http://www.ijhg.com/text.asp?2012/18/3/274/107975


Type 2 diabetes mellitus (T2DM) is a complex, polygenic, and multi-factorial disease. Both genetic predisposition and environmental factors contribute in the development and pathogenesis of T2DM. Several reports in literature have already been shown that Vitamin D deficiency may persuade to glucose intolerance, tainted insulin secretion, and finally results T2DM, suggesting the role for vitamin D in the pathogenesis of T2DM. [1] Expression and nuclear activation of the Vitamin D receptor (VDR) are necessary for the effects of vitamin D. Vitamin D plays an important role in insulin secretion. Pancreatic tissue (exclusively the insulin-producing beta-cells) expresses the VDR and allelic variations are involved in vitamin D metabolism and are associated with glucose intolerance and insulin sensitivity. [2] Interestingly, T2DM patients also have a higher incidence of hypovitaminosis D. [3] Till date, numerous genetic variations have been identified in the VDR gene and variations in this receptor have been linked to several diseases, including T2DM. [4],[5],[6],[7],[8],[9] Previously, we reported that the frequency and distribution of VDR gene variants is substantially different in diverse populations and ethnic groups. [10] Genetic studies with respect to VDR gene will definitely offer exceptional opportunities to connect molecular insights with epidemiological data and may reveal reticent and subtle but true biological effects. Collective evidences from few decades have indicated the association of many polymorphisms that exist in the VDR gene with T2DM including ours. [9] But there is no concrete conclusion or insight from the available literature that we can use the VDR variants as diagnostic tools or as a marker in future in case of T2DM. This is a big question and still a matter of debate. Additional attempts have to be initiated for better understanding of the molecular and cellular variations exaggerated by VDR gene variants including multi cohort studies; in bigger populations, special attention should be paid to correlate the effects of all the risk factors for the better understanding of the role of VDR gene variants with T2DM risk. Furthermore, the study of the different haplotypes, instead of single variant study, could eliminate some of the discrepancy found so far. Also, there is a need of more randomized clinical trial to explore the effect of Vitamin D and/or calcium supplementation with conciliator endpoints (like glucose tolerance, insulin secretion, and insulin sensitivity) and eventually with the incident of T2DM. One more prospect for better understanding of the physiological role of the vitamin-D system in diabetes is not only the insulin secretion, but also insulin resistance, which needs to be further investigated. This will increase the attention in its budding function in prevention and management of T2DM.

 
   References Top

1.Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D. Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. Diabetes Obes Metab 2008;10:185-97.  Back to cited text no. 1
    
2.Bland R, Markovic D, Hills CE, Hughes SV, Chan SL, Squires PE, et al. Expression of 25-hydroxyvitamin D3-1alpha-hydroxylase in pancreatic islets. J Steroid Biochem Mol Biol 2004;89:121-5.  Back to cited text no. 2
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3.Isaia G, Giorgino R, Adami S. High prevalence of hypovitaminosis D in female type 2 diabetic population. Diabetes Care 2001;24:1496.  Back to cited text no. 3
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4.Manchanda PK, Konwar R, Nayak VL, Singh V, Bid HK. Association of genetic variants of the vitamin D receptor (VDR) gene (Fok-I, Taq-I and Bsm-I) with susceptibility of benign prostatic hyperplasia in a North Indian population. Asian Pac J Cancer Prev 2010;11:1005-8.  Back to cited text no. 4
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5.Mittal RD, Manchanda PK, Bhat S, Bid HK. Association of vitamin-D receptor (Fok-I) gene polymorphism with bladder cancer in an Indian population. BJU Int 2007;99:933-7.  Back to cited text no. 5
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6.Mishra DK, Bid HK, Srivastava DS, Mandhani A, Mittal RD. Association of vitamin D receptor gene polymorphism and risk of prostate cancer in India. Urol Int 2005;74:315-8.  Back to cited text no. 6
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7.Bid HK, Chaudhary H, Mittal RD. Association of vitamin-D and calcitonin receptor gene polymorphism in paediatric nephrolithiasis. Pediatr Nephrol 2005;20:773-6.  Back to cited text no. 7
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8.Bid HK, Konwar R, Saxena M, Chaudhari P, Agrawal CG, Banerjee M. Association of glutathione S-transferase (GSTM1, T1 and P1) gene polymorphisms with type 2 diabetes mellitus in north Indian population. J Postgrad Med 2009;56:176-81.  Back to cited text no. 8
    
9.Bid HK, Konwar R, Aggarwal CG, Gautam S, Saxena M, Nayak VL, et al. Vitamin D receptor (FokI, BsmI and TaqI) gene polymorphisms and type 2 diabetes mellitus: A North Indian study. Indian J Med Sci 2009;63:187-94.  Back to cited text no. 9
[PUBMED]  Medknow Journal  
10.Bid HK, Mishra DK, Mittal RD. Vitamin-D receptor (VDR) gene (Fok-I, Taq-I and Apa-I) polymorphisms in healthy individuals from north Indian population. Asian Pac J Cancer Prev 2005;6:147-52.  Back to cited text no. 10
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