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Gene Expression Profiles Reveal Altered Metabolic Signaling Pathway in Skeletal Muscle With Lipid Sensor Gpr120/Ffar4

Junfeng Shi1, Taito Nakayama1, Keiko Iida1

  • 1Department of Genomic Drug Discovery Science, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|April 20, 2026
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Summary

Gpr120 deficiency reduces energy expenditure by impairing skeletal muscle mitochondrial function and gene expression. This lipid sensor is crucial for maintaining mitochondrial homeostasis and muscle strength, potentially via signaling from distant organs.

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Area of Science:

  • Metabolic regulation
  • Skeletal muscle physiology
  • Mitochondrial biology

Background:

  • Obesity stems from energy imbalance, with reduced energy expenditure (EE) a contributing factor.
  • Gpr120 (Ffar4), a lipid sensor, deficiency is linked to decreased EE.
  • Skeletal muscle is a key site for EE, making its energy metabolism critical.

Purpose of the Study:

  • To investigate the role of Gpr120 in skeletal muscle energy metabolism.
  • To determine if Gpr120 influences mitochondrial function and gene expression in skeletal muscle.

Main Methods:

  • Gene expression profiling (microarray) in WT and Gpr120-deficient mice on normal and high-fat diets.
  • Analysis of Gene Ontology (GO) term enrichment.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) for Errγ.
  • Electron microscopy for mitochondrial morphology.
  • Measurements of mitochondrial DNA (mtDNA) content and muscle strength.

Main Results:

  • Gpr120 deficiency altered mitochondrial gene expression in skeletal muscle, particularly under high-fat diet conditions.
  • GO term enrichment suggested involvement of AMPK, PGC1α, and Errγ signaling pathways.
  • Gpr120 impacts mitochondrial structure, gene expression, and function in skeletal muscle, affecting muscle strength.

Conclusions:

  • Gpr120 plays a significant role in regulating mitochondrial homeostasis and function within skeletal muscle.
  • These effects may be mediated through signaling pathways involving AMPK, PGC1α, and Errγ.
  • Gpr120's influence on skeletal muscle metabolism might be influenced by signaling originating from distant organs.