In recent years interest has been growing in the alternative physiological functions for vitamin D, asides from the traditional calcium and bone homeostasis role. Of particular interest is the role played by 25-hydroxyvitamin D [25(OH)D], the established marker for vitamin D status, in the function of the insulin receptor. Research suggests that vitamin D is associated with obesity and metabolic syndrome, but the exact cause and effects of the relationship are not fully understood. However, the ability of vitamin D to affect the insulin receptor and alter insulin secretion suggests that insulin dysfunction is the common theme that explains the role of vitamin D in obesity, metabolic syndrome and type 2 diabetes. It is known that the maternal vitamin D status affects the bone mineral density of infants born to those mothers, and research suggests that maternal vitamin D status is also able to influence infant insulin sensitivity.
For example, researchers1 have examined the association of maternal vitamin D status with anthropometric and cardiovascular risk profiles in Indian children using serum levels of 25(OH)D as a marker of vitamin D status. Measurements of 25(OH)D were taken at 28 to 32 weeks gestation in 568 women and the anthropometric measurements, glucose levels, insulin concentrations, blood pressure and fasting lipid levels were taken in the offspring at 5 and 9.5 years of age. Of the women in the study, 67% had 25(OH)D levels below 50nmol/L which suggests that vitamin D levels were suboptimal to deficient in over half of the women. Children born to vitamin D deficient women had smaller arm muscle area, when compared to children born to mothers with sufficient vitamin D status. In addition, at 9.5 years, higher fasting insulin sensitivity was lower in those children born to vitamin D deficient mothers.
The median 25(OH)D concentrations of the mothers was 39nmol/L, which considering the high sunshine climate of India, was surprisingly below the lower recommended level of ≈40nmol/L. Interestingly, there were some sex differences recorded in the study. For example in boys, maternal vitamin D deficiency was associated with higher HDL cholesterol levels, and at 5 but not 9.5 years, a higher percentage body fat with lower percentage fat free mass. However, the significance of these sex differences are not understood. Because there was no difference in grip strength between groups, but arm muscle area was smaller in children born to vitamin D deficient mothers, it is possible that the differences relates to bone circumference. However, some animal studies do show muscle growth effects for vitamin D. Taken as a whole, these results suggest that maternal 25(OH)D concentrations may have long-term implications on some physiological parameters in offspring.
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