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Protein manipulation makes obese, healthy mice

Researchers including Philipp Scherer and Christine Kusminski used protein manipulation in mice to describe links between obesity and metabolic disorders.
Manipulation of mitoNEET protein in mice's adipose tissue significantly affects obesity and glucose tolerance

Manipulating a protein in mitochondria led to mice becoming extremely obese but remaining metabolically healthy, in a new study which aimed to improve understanding of the link between the metabolic functions of obesity and its connection to type 2 diabetes.

The study, which was published in Nature Medicine, found that when levels of the protein mitoNEET were elevated inside rodent fat cell mitochondria – the part of the cell which creates ATP, the chemical which is used for metabolism in the rest of the cell – fat was stored in the adipose tissue rather than in other locations.

In effect, the researchers say, the fat acted as a “safe haven”, keeping toxic lipids away from places where they could do the most damage, like the liver.

One of the obese mice used in the study

The mice that were subjected to this treatment became enormously obese – ballooning to around five times their ordinary weight – but remained metabolically healthy.

However, in mice with artificially reduced mitoNEET levels, the mice became lean, but metabolically unhealthy, and began to demonstrate pre-diabetic conditions.

“The manipulation of mitochondrial activity in fat tissue is a very powerful approach to control how much excess energy we store in our bodies and where we store it,” said Dr Philipp Scherer, lead author and director of the Touchstone Center for Diabetes Research at the University of Texas Southwestern Medical Center. “We have heretofore underestimated the importance of mitochondrial pathways in our fat cells and their influence on how we manage our weight.”

The researchers found that mitoNEET inhibits iron from entering the mitochondria, which lowers the rate at which fatty acids are broken down in the cell to create energy.

They found an association between this effect and lower levels of cell damage from reactive oxygen species and increased production of adiponectin.

Conversely, the mice with reduced levels of mitoNEET showed higher levels of oxidative stress and glucose intolerance.

The researchers hope to conduct further studies to translate their findings into clinical applications, but for now, they say that their experiments have taught them a lot about fat cells’ role in storing and burning energy.

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