Inadequate insulin secretion leads to a rise in blood glucose levels, which is the main characteristics of diabetes. By the time a diagnosis of type 2 diabetes (T2D) is made, 70 to 80% of beta cell mass loss is already done. Loss of beta cells of pancreas occurs gradually, beginning much before the diagnosis of diabetes is made and continuing even after that. For this reason, the damage becomes irreversible (Cnop, 2005).
Skeletal benefits of vitamin D are well known and described widely in the literature, but in recent years, research has shown that Vitamin D seems to aid in preserving insulin sensitivity and insulin secretion. Circulating 25-hydroxyvitamin D (25(OH)D) concentrations disclose the levels of vitamin D in the body (Heaney, 2004). In T2D patients, this concentration is low as compared to healthy subjects (Scragg, 1995). The role of vitamin D in insulin sensitivity and insulin secretion has been hypothesized on the basis of preclinical studies (Norman, 1980). In some studies, mice and rabbits deficient in vitamin D present with impaired insulin secretion, but when supplemented with vitamin D, the defect was corrected. (Cade, 1986)
Though it is not clear how deficiency of vitamin D and diabetes is related, some researchers have suggested that there may be an autocrine/ paracrine role of vitamin D in the tissues targeting insulin. Beta cells of the islets of pancreas express the vitamin D receptor (VDR) (Johnson, 1994), which is also expressed by the skeletal tissues as well as the adipose tissue (Bischoff, 2001) that are the main determinants of peripheral insulin sensitivity. Noteworthy is that, the skeletal expression of VDR goes on reducing with age, as does the insulin sensitivity (Bischoff-Ferrari, 2004).
In a more recent study by Mitri and colleagues, it was seen that vitamin D supplementation with or without calcium improved insulin sensitivity and insulin secretion from the pancreas, which suggests that vitamin D can possible play a role in preventing or delaying the progression to clinical diabetes in population who is at a high risk of developing T2D (Mitri, 2011).
A dissertation research showed that vitamin D raises the glucose-stimulated calcium uptake, which suggests that Vitamin D is responsible for transcription of genes that are involved in calcium uptake into the beta cell of pancreas. Vitamin D status can influence the beta cells capacity to sense glucose levels and retort properly to secrete the hormone, insulin (Joyce, 2012).
In another study, particularly in T1D patients, Vitamin D was responsible for stimulating insulin secretion via regulating intracellular calcium, modulating beta-cell depolarization-stimulated insulin release, and preventing apoptosis. T1D patients had significantly low vitamin D levels (<10 ng/ml) and this was seen to be associated with higher insulin requirements suggesting an insulin secretory action of vitamin D (Gupta, 2012).
Thus, findings support the use of vitamin D in diabetes management or perhaps prevention.
References
Cnop, M., Welsh, N., Jonas, J. C., Jorns, A., Lenzen, S., Eizrik, D. L. 2005. Mechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities. Diabetes, 54, S97 – 107.
Heaney, R. P., 2004. “Functional indices of vitamin D status and ramifications of vitamin D deficiency,” The American journal of clinical nutrition, 80, no. 6, pp. 1706S–1709S.
Scragg, R., Holdaway, I., Singh, V., Metcalf, P., Baker, J., Dryson E., 1995. Serum 25-hydroxyvitamin D3 levels decreased in impaired glucose tolerance and diabetes mellitus. Diabetes Research and Clinical Practice, 27, no. 3, pp. 181–188.
Norman, A. W., Frankel, J. B., Heldt, A. M., Grodsky, G. M., 1980 Vitamin D deficiency inhibits pancreatic secretion of insulin. Science, 209, 823 –825.
Cade, C., Norman, A. W., 1986. Vitamin D3 improves impaired glucose tolerance and insulin secretion in the vitamin D-deficient rat in vivo. Endocrinology. 119, pp. 84–90.
Johnson, J. A., Grande, J. P., Roche, P. C., Kumar, R., 1994. Immunohistochemical localization of the 1,25(OH)2D3 receptor and calbindin D28k in human and rat pancreas. American Journal of Physiology, 267, no. 3, part 1, pp. E356–E360.
Bischoff, H. A., Borchers, M., Gudat, F., 2001. In situ detection of 1,25-dihydroxyvitamin D3 receptor in human skeletal muscle tissue. Histochemical Journal, 33, no. 1, pp. 19–24.
Bischoff-Ferrari, H. A., Borchers, M., Gudat, F., Durmuller, U., Stahelin, H. B., Dick, W., Vitamin D receptor expression in human muscle tissue decreases with age. Journal of Bone and Mineral Research, 19, no. 2, pp. 265–269.
Mitri J, Dawson-Hughes B, Hu F, Pittas A. (2011) Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial. American society for nutrition, 94, 486 -94. Available through: http://ajcn.nutrition.org/content/94/2/486.full [Accessed: 07th March 2013]
Joyce, R. 2012. Abstract: Role of the Vitamin D Receptor in Insulin Secretion and Beta Cell Function. UT Southwestern Electronic Theses and Dissertations. Retrieved from: https://repositories.tdl.org/utswmed-ir/handle/2152.5/1028?show=full
Gupta, V. (2012) Vitamin D: Extra-skeletal effects. J Med Nutr Nutraceut, 1, 17-26. Retrieved from: http://www.jmnn.org/article.asp?issn=2278-019X;year=2012;volume=1;issue=1;spage=17;epage=26;aulast=Gupta
