Abstract
Diabetes has become the most common metabolic disease around the world. In addition to genetic and environmental factors in adulthood, the early life environment is critical to the progression of diabetes in adults, especially the environment during the fetal period; this concept is called “fetal programming.” Substantial evidence has illustrated the key role of early life macronutrient in programming metabolic diseases. Recently, the effect of maternal micronutrient intake on offspring glucose metabolism during later life has become an emerging field. This review focuses on updated human and animal evidence about the effect of maternal micronutrient status on offspring glucose metabolism and the underlying mechanism.
Highlights
Diabetes is a serious metabolic disease and a major health concern in modern society
This review summarizes the previous studies linking maternal micronutrient surplus and deficiency and its adverse impacts on glucose metabolism in offspring and the mechanisms involved in this process
It is obvious that both maternal excess and deficiency of micronutrients affect glucose metabolism and induce insulin resistance in offspring later in life
Summary
Diabetes is a serious metabolic disease and a major health concern in modern society. In rat models, Venu et al found that maternal restriction of Mg in the diet resulted in an increase in body fat, induced insulin resistance, and impaired glucose tolerance in male pups and that rehabilitation with Mg supplementation can partially correct body composition and low-birth weight by 6 months of age [58]. Decreased expression of placental hydroxysteroid 11-beta dehydrogenase 2 (HSD11B2) was observed in pregnant women having a Zn restriction diet, which increased fetal exposure to maternal cortisol and may lead to insulin resistance and hypertension in the offspring [128]. Vitamin D deficiency during pregnancy contributed to insulin resistance and impaired glucose tolerance in male offspring, associated with increased DNA methylation of the nuclear factor κB inhibitor α (Iκbα) gene, which decreased luciferase activity [161]. BMI, body mass index; GPx, glutathione peroxidase; HDL, high-density lipoprotein; PPARγ, peroxisome proliferator-activated receptor gamma; RXR, retinoid X receptors. ↑, increased; ↓, decreased
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