Association of Serum Selenium, Zinc and Magnesium Levels with Glycaemic Indices and Insulin Resistance in Pre-diabetes: a Cross-Sectional Study from South India.

A growing understanding of antioxidant mechanisms and insulin-like actions of trace elements selenium and zinc has rekindled researchers' interest towards their role in diabetes mellitus, nutritional management of which concentrates predominantly on macronutrient intake. However, selenium studies limiting largely to diabetes have yielded inconsistent results with sparse knowledge in the pre-diabetes population. This hospital-based cross-sectional study screened 300 people who came to the institutional hospital laboratory with fasting plasma glucose and glycosylated haemoglobin requisition over a period of 6 months. Thirty-five pre-diabetes subjects aged 25-45 years and 35 age-matched healthy controls were selected as per inclusion criteria and clinical history. Serum selenium was estimated by inductively coupled plasma-mass spectrometry, zinc and magnesium by colorimetric end-point methods and insulin by enzyme-linked immunosorbent assay, and insulin resistance was calculated using a homeostasis model assessment (HOMA) 2 calculator. Data analysis was done using SPSS ver. 16 employing an independent sample t test for intergroup comparison of means and Pearson's correlation for correlation analysis. Serum mineral levels in the pre-diabetes group (selenium 63.01 ± 17.6 μg/L, zinc 55.78 ± 13.49 μg/dL, magnesium 1.37 ± 0.38 mg/dL) were significantly reduced (p < 0.05) in comparison to the healthy controls (selenium 90.98 ± 15.81 μg/L, zinc 94.53 ± 15.41 μg/dL, magnesium 2.12 ± 0.22 mg/dL). A significant negative correlation was seen with glycaemic indices and insulin resistance. This study conducted in pre-diabetes subjects highlights a considerable deficiency of serum selenium, zinc and magnesium observed at a much earlier pre-clinical phase. This coupled with the evidence of a strong inverse association with glycaemic indices and insulin resistance postulates the role of mineral alterations in the pathophysiology of hyperglycaemia and insulin resistance.