Is Vitamin D Deficiency Risk Factor for Type II Diabetes Mellitus?

Introduction Vitamin D deficiency causes reduced insulin secretion in rats and human it may predispose to glucose intolerance, altered insulin secretion and type II diabetes mellitus. The Aim of the study To study the association between vitamin D status and type II diabetes mellitus and to assess the effects of vitamin D and calcium supplementation on glycemic control. Subjects The current study included two groups the first group included 69 male diabetic patients suffering from type II diabetes mellitus and second group included 45 age and sex matched healthy persons as control group and each of this group was subdivided into 3 subgroups according treatment protocol first subgroup of each group (diabetic and control) did not receive calcium nor vit D supplementation, second subgroup of both groups receive calcium supplementation alone, third subgroup of both groups received both calcium and vitamin D supplementation. Methods all subjects of the study was subjected to careful history taking, thorough clinical examination, laboratory investigation including fasting and two hours postprandial blood sugar, Fructosamine, Fasting Insulin, & HOMA-IR in addition to Vitamin D assessment by ELIZA in the beginning and after one month of starting treatment protocol. Results Serum Vitamin D and fasting insulin levels were statically higher among control group than among diabetic patients as whole while mean values of other parameters were statically higher compared to controls. Statistically significant decrease of serum vitamin D and fasting insulin levels and statistically significant increase of FBG, PPBG, serum fructosamin and HOMA. IR were found in diabetic group as compared to control group as a whole in the beginning of study and after one month of supplement of calcium and vitamin D in 2nd and 3rd subgroups of both group, there was statistically significant decrease of FBG, PPBG, serum fractosamin and HOMA. IR and significant increase of serum insulin level in the 2nd and 3rd subgroups of diabetic patients after one month of treatment protocol as compared to before treatment, while serum vitamin D was significant increase in subgroup III only after treatment with calcium and vitamin D. Significant negative correlation between vitamin D and each of FBS, PPBG, serum fractosamin and HOMA IR and significant positive correlation between vitamin D and serum fasting insulin in diabetic subgroup III. Conclusion vitamin D deficiency may play role in development of type II diabetes in susceptible individuals and its supplementation to those subjects improve glycemic status thus correction of vitamin D deficiency of those subjects may delay or prevent occurrence of type II diabetes and help to improve glycemic control of type II diabetes but our understanding of the exact mechanisms by which vitamin D and calcium may promote beta cell function, or ameliorate insulin resistance and systemic inflammation is in need for more investigation.