Cell Subsidiary: Duke University discovers new targets for fatty liver and pre-diabetes

Cell Subsidiary: Duke University discovers new targets for fatty liver and pre-diabetes

May 29, 2018 Source: WuXi PharmaTech

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Recently, Duke University scientists have discovered a pathway in the liver that they believe can be used to reduce fat deposition in the liver by balancing the two interacting enzymes to control fat metabolism. When they tried this method in a rat model of obesity and metabolic disease, they found that they could reduce the amount of fat deposited in the liver and improve glucose regulation. The results were published in the famous journal Cell Metabolism.

According to the American Liver Foundation, fat accumulates in the liver to form nonalcoholic fatty liver disease (NAFLD), which currently affects up to 25% of Americans. As the rate of obesity increases, the trend of this disease is also increasing. People in pre-diabetes have a higher risk of developing NAFLD and there is no cure.

The key to this discovery from Duke University is branched-chain amino acids (BCAA), which are produced during protein metabolism. Scientists have long known that there is a link between BCAA, obesity, and insulin resistance, but they have been trying to figure out the mechanisms behind this connection. Therefore, researchers at the Institute of Molecular Physiology at Duke University hope to focus on two enzymes that control the breakdown of BCAA in vivo: one is a kinase that inhibits breakdown, and the other is a phosphatase that activates it.

First, they tested kinase inhibitors developed by the University of Texas Southwestern Medical Center in a rat model. Then they found a way to activate phosphatase. Both experiments produced the same results: reduced liver fat and better glycemic control. And these improvements began to appear within a week.

â–² Dr. Phillip White, Assistant Professor, Institute of Molecular Physiology, Duke University (Source: Duke Molecular Physiology Institute)

"This particular rat model (Zucker fat mouse) is an extreme model of obesity and metabolic disease, so it would be important if it could be improved within a week," said Dr. Phillip White, lead author of the study.

This is the latest example of a new insight into enzyme activity that promotes research on diabetes and related diseases. In March of this year, a team at Columbia University demonstrated in rodents that insulin resistance can be improved if they turn off the production of DPP4 enzymes in the liver. A study by a Japanese team in a study published in January showed that Sir2 may be a target for improving glucose uptake in the liver.

Duke's research team is planning to conduct further experiments to better understand how BCCA targets fatty liver disease and pre-diabetes. But the results they observed in Zucker's fat mice have spurred some experts to consider new strategies for treating metabolic disorders.

“There is increasing evidence that BCAA may not just be a passive marker of diabetes, it actually plays a role in the pathogenesis process,” Clinical and Translational Research, Heart Center, Massachusetts General Hospital Dr. Robert Gerszten, Director, said: "It gives us the motivation to decide whether it is worth exploring the changes in amino acid intake in the diet."

Reference materials:

[1] Duke team IDs new target for fatty liver disease and prediabetes

[2] Diabetes researchers find switch for fatty liver disease

[3] The BCKDH Kinase and Phosphatase Integrate BCAA and Lipid Metabolism via Regulation of ATP-Citrate Lyase

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