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Objective: We investigated the association of dietary magnesium intake with insulin resistance and markers of endothelial function among Iranian women. Design: A cross-sectional study. Setting: Usual dietary intakes were assessed using a validated food frequency questionnaire. Dietary magnesium intake was calculated by summing up the amount of magnesium in all foods. A fasting blood sample was taken to measure serum concentrations of glycemic indices (fasting plasma glucose and insulin) and endothelial function markers (E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1). Insulin resistance and sensitivity were estimated using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR), Homeostasis Model Assessment β-cell function (HOMA-β) and quantitative insulin sensitivity check index (QUICKI), respectively. Participants: Iranian female nurses (n=345) selected by a multistage cluster random sampling method. Results: The magnesium intake across energy-adjusted quartiles was 205±7 (mean±SE), 221.4±8, 254.3±7 and 355.2±9 mg/d, respectively. After adjustments for potential confounders, QUICKI level was significantly different across quartiles of magnesium intake (Q1: 0.34±0.02, Q2: 0.36±0.01, Q3: 0.40±0.01, Q4: 0.39±0.02, P=0.02); however, this association disappeared after considering markers of endothelial function; indicating that this relation might be mediated through endothelial dysfunction. After controlling for all potential confounders, magnesium intake was inversely, but not significantly, associated with serum concentrations of sICAM (Q1: 239±17, Q2: 214±12, Q3: 196±12, Q4: 195±17, P=0.29). There was no other significant association between dietary magnesium intake and other indicators of glucose homeostasis or endothelial markers. Conclusions: Higher dietary magnesium intake was associated with better insulin sensitivity in Iranian females. This linkage was mediated through reduced endothelial dysfunction.

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