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05-26-2020

Cellular response to fasting may be key to promoting weight loss

Researchers at the University of Warwick have discovered how the body responds to fasting to induce autophagy. This process promotes enormous health benefits on a cellular level, including weight loss.

The study has major implications for the development of new treatments to help people who struggle with obesity. 

The obesity epidemic has grown rapidly across America over the last two decades, jumping from a rate of 30 percent in 2000 to 42 percent by 2019. In the UK, it is estimated that more than half the population will be obese by the year 2050. 

While some people are genetically predisposed to obesity, the condition is primarily caused by adjustable lifestyle factors such as sedentary behavior and high-calorie diets.

Many people turn to calorie restriction and fasting diets to maintain a healthy weight. 

In response to fasting, cells go into preservation mode and launch a process known as autophagy, where genes are switched on to clean out old, unnecessary material and proteins that build up inside of cells.

Beyond cell renewal, autophagy genes have been linked to incredible health benefits including weight loss, lower heart disease risk, longevity, and tumor prevention. 

In the Warwick study, researchers led by Professor Ioannis Nezis identified the proteins that are required to switch on autophagy and its cellular recycling pathway.

The team found that three proteins – Sequoia, YL-1, and Sir2 – recruit the autophagy-related protein Atg8a in the cell nucleus to control the transcription of autophagy genes. 

The study is the first to uncover a nuclear role of the cytoplasmic protein Atg8a.

“Understanding the molecular mechanisms of activation of autophagy genes during fasting will help us to use interventions to activate the autophagic pathways to maintain a normal body weight and promote healthy well-being,” said Professor Nezis.

The study is published in the journal Cell Reports.

By Chrissy Sexton, Earth.com Staff Writer

 

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