Sure, foods that are high in sugar are often the most tempting, but that sugar rush can come at a weighty cost. A new study conducted at the University of South Carolina has suggested that this may not need be the case. Researchers have identified a gene that can dictate how these foods are processed, potentially suppressing the weight problems that go hand-in-hand with unhealthy eating habits.
The research centers on a mutant gene called SKN-1 found in the worm Caenorhabditis elegans. The scientists fed a number of these worms a high-sugar diet and observed no difference in weight for those with a hyperactive SKN-1 gene, while those without the gene quickly began to stack on the nanograms.
This mutant gene is present in humans, though it goes by the name of Nrf2. Described as a "transcriptor factor," the gene clings to a particular DNA sequence and aids in our cells' ability to detox or repair themselves when damaged by chemically reactive oxygen. These properties have seen the gene become a target for pharmaceutical companies, who anticipate a role in it producing anti-oxidants and helping to slow aging.
The team is hopeful that the positive effects of the mutant gene in the worms will also apply to humans. But don't start cooking up that Deep Fried KitKat Grilled Cheese Sandwich just yet. The research so far has been limited to the worms and human cells in a petri dish. Furthermore, heightened Nrf2 function has been linked to aggressive cancers in humans, suggesting there's quite a bit to work through before this research culminates in a drug that enables guilt-free gorging.
“Perhaps it is a matter of timing and location,” says Sean Curran from USC Davis School of Gerontology and leader of the research. “If we can acutely activate Nrf2 in specific tissues when needed then maybe we can take advantage of its potential benefits.”
The team's research was published in the journal Nature Communications.
Source: University of South Carolina
Want a cleaner, faster loading and ad free reading experience?
Try New Atlas Plus. Learn more