Maternal Zinc and Metabolic Syndrome

Findings from a recent study suggest suboptimal maternal zinc status induces long-term changes in the offspring related to abnormal glucose tolerance (J Nutr. 2010; 140(9):1621-1627). Maternal zinc deficiency affects maternal carbohydrate metabolism, but the mechanisms underlying changes in glucose homeostasis of offspring are not well understood. Rats consumed zinc-deficient (7 mug/g) or control (25 mug/g) diets ad libitum from three weeks preconception to 21 day postparturition. Litters were culled to 7 pups/dam postnatally and pups were allowed to nurse their original mothers; after weaning, pups were fed a non-purified diet. Insulin and glucose tolerance tests were performed on the pups at weeks five and 10.Although there was no difference in birth weight between groups, zinc-deficient pups weighed significantly more than controls by day 10 and 20. Both blood glucose and serum insulin-like growth factor (IGF-1) concentrations at week three were significantly higher in zinc-deficient pups than in controls. Both male and female zinc-deficient rats were less sensitive to insulin and glucose stimulation than controls at week five and 10. At week 15, serum leptin concentrations were higher in male zinc-deficient rats than in controls. Phosphorylation of muscle Akt protein, an insulin receptor (IR) signaling intermediate, was lower in female zinc-deficient rats than in controls at week 15, but they did not differ in phosphorylation of IR. Maternal zinc deficiency resulted in greater serum IGF-1 concentrations and the excessive postnatal weight gain in their offspring as well as impaired subsequent glucose sensitivity. It was associated with gender-specific alterations in the serum leptin concentration and the insulin signaling pathway.

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