Retarded fetal growth may lead to type 2 diabetes in adult life, according to a new study from University of Pennsylvania, Philadelphia.
The study led by Rebecca Simmons suggested that Intrauterine growth retardation (IUGR), which results in a baby having a low weight at birth may be linked to diabetes in adulthood.
This is because the expression of key genes is altered during fetal development, which affects disease susceptibility.
Prior studies conducted using a rat model of IUGR have shown decreased fetal expression of the gene Pdx1, which is critical for the development and function of the cells that become defective in type 2 diabetes (pancreatic beta-cells), and adult onset of diabetes.
The present study also conducted using rat model of IUGR found that the expression of Pdx1 was reduced in pancreatic beta-cells throughout life following IUGR.
The molecular mechanisms (known as epigenetic mechanisms because they affect gene expression without altering the information in the gene) that reduced Pdx1 expression in pancreatic beta-cells were found to change during development.
One mechanism was observed in the fetus, one following birth, and one after the onset of diabetes in adulthood.
However, the study also suggested that the mechanisms reducing Pdx1 gene expression in the fetus and following birth could be reversed, whereas those reducing Pdx1 gene expression in the adult were irreversible.
These data provide new insight into the mechanisms by which diabetes develops in adulthood following IUGR.
The study appears in Journal of Clinical Investigation.