A gene named HHEX/IDE, which has already been implicated in the development of type 2 diabetes (see research article), may also contribute to childhood obesity. While the gene does not appear to affect birth weight and does not necessarily predispose an adult to become obese, it may set the stage for obesity in some children.
Researchers investigated 20 gene variants, or single nucleotide polymorphisms (SNPs or “snips”) previously associated with type 2 diabetes. A genetic polymorphism (from Ancient Greek; poly = many, morph = form) occurs when there are two or more forms of the same gene. This is caused by a single nucleotide substitution or deletion in the sequence of nucleotides that code for the gene. It’s like substituting the letter “h” for the letter “c” in the word “cat,” changing the word to “hat,” which is something completely different.
SNPs are important in genetic research because of the comparisons that can be made between two groups (such as one group with a disease, and one without). Do the members of the group with a disease all have SNPs in the same region of their genetic code? If so, then we can assume that the gene in which the SNPs occur may be involved in a given disease.
Using a group of 7,200 children involved in an ongoing study of childhood obesity, researchers found that the HEX/IDE gene makes it more likely that a child will become obese during childhood.
In the press release from The Children’s Hospital of Philadelphia, study leader Struan F.A. Grant, Ph.D., a researcher and Associate Director of the Center for Applied Genomics of the hospital, says, “It has been a bit of a mystery to scientists how or even if these adult diabetes genes function during childhood. This finding suggests that there may be genetic activity during childhood that lays the foundation for the later development of type 2 diabetes…Previously we thought that this gene affects insulin production during adulthood, but we now see that it may play an early role in influencing insulin resistance through its impact on body size during childhood. One implication is that if we can develop medicines to target specific biological pathways in childhood, we may be able to prevent diabetes from developing later in life.”
The finding is important not only in elucidating the genetic origins of diabetes, but may present an avenue for developing drugs to counteract the disease.
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Children’s Hospital press release
Research Article abstract