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Objective: Lower levels of selenium and vitamin E have been described in gestational diabetes, a condition similar to type 2 diabetes, but few data are available about zinc (known to be associated with diabetes) and gestational hyperglycemia. This study evaluated the dietary intake of antioxidant vitamins, zinc, selenium, and serum levels of zinc and selenium in women with gestational hyperglycemia and normoglycemia., Methods: A food-frequency questionnaire was administered to 504 pregnant women (210 with hyperglycemia and 294 with normoglycemia). Serum levels of zinc and selenium were analyzed during pregnancy in a second cohort of 71 hyperglycemic and 123 normoglycemic women, with a mean age and body mass index similar to those in the first cohort., Results: Dietary intakes of zinc and selenium were significantly lower in hyperglycemic patients. In multiple logistic regression analysis, intakes were negatively associated with gestational hyperglycemia (odds ratios of 0.89 for zinc and 0.97 for selenium) after multiple adjustments. There were no significant differences in vitamin intakes. In the second cohort of 194 patients, serum levels of zinc and selenium were significantly lower in patients who had impaired glucose tolerance and negatively associated with gestational hyperglycemia in a multiple logistic regression model (odds ratios of 0.93 for serum zinc and 0.92 for serum selenium)., Conclusions: Our data suggested a significant inverse association of dietary intakes and serum levels of zinc and selenium with gestational hyperglycemia. If future studies confirm these results, it might be a useful interventional approach to appropriate dietary counseling in order to evaluate the possible decrease in gestational metabolic abnormalities and their adverse consequences.

Inhibition of tumor necrosis factor-alpha (TNF-alpha) represents a relevant target in rheumatoid arthritis therapy. Besides inhibiting cyclooxygenase, anti-inflammatory drugs can affect the activation of transcription factors. We investigated the ability of dexamethasone, indomethacin, and rofecoxib to modulate nuclear factor-kappaB (NF-kappaB) activation and TNF-alpha release from human monocytes challenged with lipopolysaccharide (LPS) or phorbol 12-myristate 13-acetate (PMA). Both stimuli induced NF-kappaB nuclear translocation and TNF-alpha secretion. Dexamethasone potently inhibited TNF-alpha release, indomethacin inhibited only PMA-evoked release, while rofecoxib had no effect. In the electrophoretic mobility shift assay, dexamethasone and rofecoxib dose-dependently inhibited the DNA binding activity of NF-kappaB in stimulated monocytes, whereas indomethacin failed to inhibit the LPS-evoked one. These results were further confirmed by evaluating the drugs' ability to reduce nuclear NF-kappaB subunits, as well as the amount of phosphorylated IkappaBalpha in cytosolic fractions. In conclusion, these results indicate that anti-inflammatory drugs differ largely in their ability to inhibit NF-kappaB activity and/or TNF-alpha release from human monocytes. These effects can be relevant to rheumatoid arthritis therapy.