Linking the Genetics of Type 2 Diabetes With Low Birth Weight
A Role for Prenatal Islet Maldevelopment?
- Department of Medicine I, St. Josef-Hospital, Ruhr-University of Bochum, Bochum, Germany.
- Corresponding author: Juris J. Meier, juris.Meier{at}ruhr-uni-bochum.de.
Diabetes develops if pancreatic β-cells fail to provide sufficient amounts of insulin at a given degree of insulin resistance. In type 1 diabetes, the extent of β-cell loss at the time of disease onset has been estimated to be ∼60–70% (1,2), while studies in patients with type 2 diabetes and individuals with impaired fasting glucose have reported β-cell deficits of ∼65 and ∼50%, respectively (3). However, while impaired islet cell mass and function seem to determine the development of diabetes to a large extent, individual risk undoubtedly also depends on other parameters, such as obesity and insulin resistance (4).
Over the years, increasing evidence has accumulated that shows that, in addition to these established risk factors, low birth weight is also associated with a greater risk of developing type 2 diabetes later in life (5,6). The causes underlying this association have been debated, and fetal malnutrition has been proposed as a potential mechanism (7,8).
Freathy et al. (9), as reported in this issue of Diabetes, have now tested the alternative hypothesis (the fetal insulin hypothesis) that genetic variants predisposing to type 2 diabetes might also reduce birth weight by altering intrauterine insulin secretion or action. Using fetal DNA from 7,986 mothers and …
