September 20, 2012
Micro-RNA Causes Metabolic Issues In People With Obesity
Scientists have identified a key molecular player in a chain of events in the body that can lead to fatty liver disease, Type II diabetes and other metabolic abnormalities associated with obesity. By blocking this molecule, the researchers were able to reverse some of the pathology it caused in obese mice.
Their findings appear in the Proceedings of the National Academy of Sciences.
In response to signals from the small intestine, beta-Klotho contributes to normal liver function after a meal, said University of Illinois molecular and integrative physiology professor Jongsook Kim Kemper, who led the study. But in obesity, levels of miR-34a surge much higher than normal, resulting in abnormally low levels of beta-Klotho.
"The downstream effect is more glucose in the blood, more fat in the liver," she said.
The effects are dramatic. Slices of liver tissue from obese mice are laden with fat, whereas normal mice have minimal amounts of fat in their livers.
The researchers used a complementary strand of RNA (called antisense RNA) to neutralize miR-34a in obese mice. This therapeutic approach improved "metabolic outcomes, including decreased liver fat and improved glucose level in the blood," Kemper said.
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