Time-restricted eating could prevent obesity-related muscle dysfunction

The researchers then checked the metabolism, muscular strength, and gene expression in fruit flies at times when they were flying. They found that members of the second group experienced reduced insulin resistance, decreased intramuscular fat, and improved muscle quality as a result of TRF.

They also noticed low levels of fat-processing enzymes that increase the risk of a heart attack in humans. Plus, there was an increase in the activity of genes associated with the production of glycine, an amino acid that benefits the metabolism of the human body.

Although the approach hasn’t been tested on humans yet, the findings of the current study suggest that TRF could emerge as an effective means of treating the various ill effects of obesity in overweight individuals.

“Our mechanistic approach — along with interventions including time-restricted eating — will be highly useful in addressing and treating the obesity, cardiovascular disease, and dementia disparities seen in the Deep South,” said Professor Melkani.

The study is published in the journal Nature Communications.

Study Abstract: 

Obesity caused by genetic and environmental factors can lead to compromised skeletal muscle function. Time-restricted feeding (TRF) has been shown to prevent muscle function decline from obesogenic challenges; however, its mechanism remains unclear. Here we demonstrate that TRF upregulates genes involved in glycine production (Sardh and CG5955) and utilization (Gnmt), while Dgat2, involved in triglyceride synthesis, is downregulated in Drosophila models of diet- and genetic-induced obesity. Muscle-specific knockdown of Gnmt, Sardh, and CG5955 leads to muscle dysfunction, ectopic lipid accumulation, and loss of TRF-mediated benefits, while knockdown of Dgat2 retains muscle function during aging and reduces ectopic lipid accumulation. Further analyses demonstrate that TRF upregulates the purine cycle in a diet-induced obesity model and AMPK signaling-associated pathways in a genetic-induced obesity model. Overall, our data suggest that TRF improves muscle function through modulations of common and distinct pathways under different obesogenic challenges and provides potential targets for obesity treatments.

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