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High-sugar diet no problem for genetic mutants

Date:
October 6, 2014
Source:
University of Southern California
Summary:
A genetic pathway for circumventing the weight gain that accompanies a high-sugar diet has been discovered by scientists. Building on previous work with C. elegans, researchers found that certain genetic mutants -- those with a hyperactive SKN-1 gene -- could be fed incredibly high-sugar diets without gaining any weight, while regular C. elegans ballooned on the same diet.
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Imagine being able to take a pill that lets you eat all of the ice cream, cookies, and cakes that you wanted -- without gaining any weight.

New research from USC suggests that dream may not be impossible. A team of scientists led by Sean Curran of the USC Davis School of Gerontology and the Keck School of Medicine of USC found a new way to suppress the obesity that accompanies a high-sugar diet, pinning it down to a key gene that pharmaceutical companies have already developed drugs to target.

So far, Curran's work has been solely on the worm Caenorhabditis elegans and human cells in a petri dish -- but the genetic pathway he studied is found in almost all animals from yeast to humans. Next, he plans to test his findings in mice.

Curran's research is outlined in a study that will be published on Oct. 6 by Nature Communications.

Building on previous work with C. elegans, Curran and his colleagues found that certain genetic mutants -- those with a hyperactive SKN-1 gene -- could be fed incredibly high-sugar diets without gaining any weight, while regular C. elegans ballooned on the same diet.

"The high-sugar diet that the bacteria ate was the equivalent of a human eating the Western diet," Curran said, referring to the diet favored by the Western world, characterized by high-fat and high-sugar foods, like burgers, fries and soda.

The SKN-1 gene also exists in humans, where it is called Nrf2, suggesting that the findings might translate, he said. The Nrf2 protein, a "transcription factor" that binds to a specific sequence of DNA to control the ability of cells to detox or repair damage when exposed to chemically reactive oxygen (a common threat to cells' well being), has been well studied in mammals.

Pharmaceutical companies have already worked to develop small-molecule drugs that target Nrf2, in hopes that it will produce more anti-oxidants and slow aging.

Though the promise of a pill to help control your body's response to food is enticing, it is not without risk, Curran said. Increased Nrf2 function has been linked to aggressive cancers.

"Perhaps it is a matter of timing and location," Curran said. "If we can acutely activate Nrf2 in specific tissues when needed then maybe we can take advantage of its potential benefits."


Story Source:

Materials provided by University of Southern California. Note: Content may be edited for style and length.


Journal Reference:

  1. Shanshan Pang, Dana A. Lynn, Jacqueline Y. Lo, Jennifer Paek, Sean P. Curran. SKN-1 and Nrf2 couples proline catabolism with lipid metabolism during nutrient deprivation. Nature Communications, 2014; 5: 5048 DOI: 10.1038/ncomms6048

Cite This Page:

University of Southern California. "High-sugar diet no problem for genetic mutants." ScienceDaily. ScienceDaily, 6 October 2014. <www.sciencedaily.com/releases/2014/10/141006133502.htm>.
University of Southern California. (2014, October 6). High-sugar diet no problem for genetic mutants. ScienceDaily. Retrieved February 26, 2024 from www.sciencedaily.com/releases/2014/10/141006133502.htm
University of Southern California. "High-sugar diet no problem for genetic mutants." ScienceDaily. www.sciencedaily.com/releases/2014/10/141006133502.htm (accessed February 26, 2024).

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