A gene previously shown to be involved in the development of type 2 diabetes also predisposes children to having a lower birth weight, a new study has found.
The study, by researchers from The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, sheds light on a possible genetic influence on how prenatal events may set the stage for developing diabetes in later childhood or adulthood.
The research has been published in the online version of the journal Diabetes.
"It's a bit unusual to find a gene linked to both prenatal events and to a disease that occurs later in life," said study leader Struan F.A. Grant, Ph.D., a researcher at the Center for Applied Genomics of The Children's Hospital of Philadelphia.
"This gene variant carries a double whammy, in raising the risk of both lower birth weight and the development of type 2 diabetes in later life," the expert said.
Type 2 diabetes occurs either when the pancreas produces too little insulin or when the body cannot efficiently use the insulin that is produced. Formerly called adult-onset diabetes and still most common in adults, type 2 diabetes has been increasing sharply among children.
To reach the conclusion, Grant and study co-leader Hakon Hakonarson, Ph.D., director of the Center for Applied Genomics at Children's Hospital, investigated 20 gene locations previously reported to be associated with type 2 diabetes. Drawing on a cohort of some 5,700 Caucasian children in an ongoing genome-wide association study of childhood obesity at Children's Hospital, the researchers compared birth weights with the occurrence of the 20 gene variants.
They found that one of the gene variants, called CDKAL1, had a strong association with lower birth weight-a finding that supports the so-called fetal insulin hypothesis.
Under the fetal insulin hypothesis, a slight underproduction of insulin, an important fetal growth factor, during the prenatal period may cause a baby to be born smaller. Low birth weight is already known to increase the risk of disease later in life, and the fetal insulin hypothesis proposes that the same gene that causes lower birth weight also increases the risk of developing type 2 diabetes.