Download Abstract - Mediterranean Group for the Study of Diabetes

DIABETES AND VITAMIN D
Stefania Maggi
CNR Aging Branch, Institute of Neuroscience, Padova, Italy
Several clinical and epidemiologic studies suggest a link between vitamin D deficiency early
in life and the development of Type 1 Diabetes (T1D). In particular, such association seems to
be related to the immunomodulatory actions of vitamin D. Vitamin D receptors (VDR) have
been identified in pancreatic  cells and some studies reported that the development of T1D is
associated with polymorphisms in the VDR gene.1 Moreover, the EURODIAB Study found
that vitamin D supplementation early in life reduces significantly the risk of developing
T1D.2 More recently, a large number of observational studies have also suggested an
association between Type 2 Diabetes (T2D) and Vitamin D deficiency. The prevalence of
vitamin D deficiency is very high, not only in the older T2D patients, but also in younger
patients. A very interesting study has reported a lower vitamin D concentration and a higher
prevalence of T2D in a London Bangladeshi population compared to British Caucasians,
suggesting that vitamin D status might contribute to the pathogenesis of the disease.
Moreover, vitamin D supplementation has been shown to increase insulin secretion and also
to improve glucose levels.3 Evidence exists that vitamin D facilitates the conversion of
proinsulin to insulin through a rise in intracellular calcium concentration. We know that
vitamin D supplementation in the early stages of experimental vitamin D deficiency leads to a
partial improvement in insulin sensitivity. Recent findings suggest that this improvement
might be due to the ability of vitamin D to inhibit CEACAM1, a negative regulator of insulin
action.4 It is known that VDRs are present also in activated T lymphocytes, macrophages and
thymus tissue and this demonstrates that vitamin D has a role in the immuno-modulation.
Vitamin D has been reported to down-regulate the production of inflammatory factors (e.g.
TNF-α and TNF-β, IL-6, IL-2) that have often been associated with insulin resistance and βcell failure.5 Finally, Vitamin D is deposited in body fat stores and, therefore, obese persons,
as most of T2D patients are, have often a chronic deficiency in vitamin D bioavailability.6 In
conclusion, the relationship between hypovitaminosis D, altered insulin synthesis, secretion
and action may be the result of several related metabolic effects. We need adequate
randomized trials to determine whether Vitamin D really is the promising, new element in the
prevention and management of diabetes that observational studies seem to suggest.
1. Knip M, Virtanen SM, Akerblom HK. Infant feeding and the risk of type 1 diabetes. Am J
Clin Nutr. 2010 May;91(5):1506S-1513S
2. Soltesz G, Patterson CC, Dahlquist G; EURODIAB Study Group Worldwide childhood
type 1 diabetes incidence--what can we learn from epidemiology? Pediatr Diabetes. 2007
Oct;8 Suppl 6:6-14
3. Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence? Br J Nutr
2003; 89:552-572
4. Liu W, Guo M, Ezzat S, Asa SL.Vitamin D inhibits CEACAM1 to promote insulin/IGF-I
receptor signaling without compromising anti-proliferative action. Lab Invest. 2010 Aug
16
5. Mathieu C, van Etten E, Decallonne B, et al. Vitamin D and 1,25-dihydroxyvitamin D3 as
modulators in the immunesystem. J Steroid Biochem Mol Bio 2004; 89–90: 449–52
6. Boucher BJ. Vitamin D insufficiency and Diabetes Risks. Curr Drug Targets.2010 Aug 27