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Time-restricted feeding promotes muscle function through purine cycle and AMPK signaling in Drosophila obesity models. | LitMetric

AI Article Synopsis

  • Obesity, influenced by both genetic and environmental factors, negatively affects skeletal muscle function, but time-restricted feeding (TRF) may help prevent this decline.* -
  • TRF appears to enhance the production and utilization of glycine-related genes while reducing triglyceride synthesis genes, and specific gene knockdowns can lead to muscle dysfunction and loss of TRF benefits.* -
  • The findings suggest that TRF may improve muscle function by altering distinct metabolic pathways, offering promising targets for obesity treatments.*

Article 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 lead 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9944249PMC
http://dx.doi.org/10.1038/s41467-023-36474-4DOI Listing

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