In this study no statistically significant difference was found in serum zinc levels between children and adolescents with TIDM and healthy controls. Several studies on animal models of diabetes and humans with diabetes have been reported in the literature in which plasma or serum zinc concentration has been used as an indicator of zinc status, but the results have been contradictory (3
). Furthermore, there are very few studies specifically on children and adolescents with T1DM, and these studies show contradictory results (10
). Our results confirm the findings of some studies (14
), in which no difference in serum zinc concentration was observed between children and adolescents with T1DM and healthy controls. However, some investigators have reported lower (10
) or higher (12
) serum zinc levels in T1DM children. Probable reasons for these contradictory findings could be differences in the presence or absence of glycemic control, duration of diabetes, or the amount of zinc intake among the patients. However, in this study no correlations were found between serum zinc levels and HbA1c
or the duration of the disease. Jansen et al. (20
) have hypothesized that the plasma zinc concentration may be related to the duration of the disease, such that the initial elevation of the plasma levels at the onset of the disease (when beta cell destruction occurs) is followed afterwards by a drop when elevated urinary zinc excretion overcomes the release of zinc from beta cells. This hypothesis is supported by the negative correlation between the duration of T1DM and plasma/serum zinc concentration in some studies (3
). However, in our study no significant correlation was found between the two variables. Even when we subdivided the diabetics according to their duration of the disease, nothing changed.
The possible relationship between zinc and diabetes mellitus has been of interest to many investigators since it was understood that zinc was part of the insulin complex. The most consistent finding of the animal and human studies on this subject so far is hyperzincuria (20
). This has prompted some scientists to advance hypotheses stating that diabetics may develop zinc deficiency. However, none of our patients was zinc-deficient. It is to be noted that the assessment of borderline zinc deficiency is more difficult due to the non-existence of frank clinical signs and reliable, well-defined, sensitive and specific laboratory indicators. In contrast to some other nutrients, there are no zinc reserves in the human body. As a result, when there is an insufficient dietary intake of zinc, problems can be expected. For example, the growth rate in children or the zinc excretion in adults is reduced in an effort to maintain zinc levels of tissues and homeostasis; consequently no apparent biochemical or functional changes occur (22
). In our study, 62.1% of the patients and 60% of the healthy controls had a low zinc intake compared to the respective RDA. Thus, despite normal serum zinc levels the possibility of borderline zinc deficiency in both groups cannot be ruled out.
In conclusion, the serum zinc levels of these diabetic children and adolescents were not noticeably different compared to those of healthy controls and were independent of glycemic control and the duration of the disease. Diabetic patients were not zinc-deficient based on their serum levels, despite the fact that the dietary zinc intake of about 60% of them was low. Certainly more research is required to shed more light on the subject.