New York:
Researchers have identified a genetic variant that regulates hundreds of genes that govern how and where women's bodies store fat, which affects their risk of developing Type-2 diabetes.
The variant is located near the KLF14 gene, which encodes a protein that directly regulates the expression of hundreds of other genes in fat tissue.
Specifically, the researchers found that different alleles, or versions, of the variant cause fat-storing cells to function differently.
"Previous studies have shown that on average, women who carry fat in their hips -- those with a 'pear-shaped' body type -- are significantly less likely to develop diabetes than those with smaller hips," said study lead author Kerrin Small King's College London.
"Looking at the variant we studied, large-scale genome-wide association studies show that women with one allele tend to have larger hips than women with the other one, which would have a protective effect against diabetes," she said.
KLF14 is maternally imprinted, which means that a person's expression of KLF14 and the resulting effects on fat tissue are determined by the version of the gene inherited from his or her mother -- the father's allele does not affect levels of this regulatory protein.
Researchers first identified the relationship between the variant near KLF14 and Type-2 diabetes risk in a large, genome-wide association study of a broad population.
As with most studies of this type, the effect on diabetes risk was modest, though statistically significant.
However, when Small and her colleagues focused on a more specific population, women who inherited the allele from their mothers, the effect size grew.
"These findings have important implications as we move toward more personalised approaches to disease detection and treatment," Small said.
"If we can identify the genes and protein products involved in diabetes risk, even for a subset of people, we may be able to develop effective treatment and prevention approaches tailored to people in that group," she pointed out.
The findings were presented at the American Society of Human Genetics (ASHG) 2015 annual meeting in Baltimore, Maryland.