Apple or pear? Scientists discover new gene linked to your body shape

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WASHINGTON — Scientists have found a new gene linked to body fat distribution in research that may help explain why you have an apple or pear shape.

Researchers from the Duke University reported Monday in the U.S. journal Proceedings of the National Academy of Sciences that a gene called Plexin D1 could control both where fat is stored and how fat cells are shaped, known factors in health and even the risk of future disease.

“This work identifies a new molecular pathway that determines how fat is stored in the body, and as a result, affects overall metabolic health,” said senior author John Rawls, associate professor of molecular genetics and microbiology at Duke University School of Medicine. “Moving forward, the components of that pathway can become potential targets to address the dangers associated with visceral fat accumulation.

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The researchers chose zebrafish for this study since their transparent bodies were easy to observe and found those genetically engineered to lack Plexin D1 had less abdominal or visceral fat, the kind that lends some humans a characteristic apple shape, than their normal counterparts.

Previous research has shown that people with an apple shape are more likely to develop diabetes and heart disease than those who have bigger hips and thighs, also described as being pear-shaped.

The same effect was observed in zebrafish. Those who were knocked out of the gene were protected from insulin resistance, a precursor of diabetes, even after eating a high-fat diet.

And that may be because that the visceral fat tissue of the mutant zebrafish was composed of smaller, but more numerous cells, which the researchers said are known to decrease the risk of insulin resistance and metabolic disease in humans.

In contrast, their normal siblings had visceral fat tissue containing larger, but fewer fat cells of the kind known to be more likely to leak inflammatory substances that contribute to illness.

Bolstering the zebrafish findings, collaborators at the Karolinska Institute in Sweden analyzed human patient samples and showed that levels of Plexin D1 were higher in individuals with type 2 diabetes, suggesting it may play a similar role in humans.

The researchers also used mice to study the function of Plexin D1, but all of the animals altered to lack the gene died at birth.

Next, they planned to search for other genes as well as environmental factors that are involved in the biology of body fat, again using zebrafish models.

“Our results indicate that the genetic architecture of body fat distribution is shared between fish and humans, which represents about 450 million years of evolutionary divergence,” Rawls said. ” For these pathways to have been conserved for so long suggests that they are serving an important role.”