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Updated: Jun 17, 2026

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
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Body Composition and Metabolic Caging Analysis in High Fat Fed Mice

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Rsk4 Mediates Brain FGF19 Signaling to Constrain Diet-Induced Obesity in Mice.

Chaonan Li1,2, Kaiyue Gu1,2, Ying Huang1,2

  • 1Institute of Metabolism and Health, Department of Pathophysiology, School of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.

Diabetes
|June 16, 2026
PubMed
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Ribosomal S6 kinase 4 (Rsk4) loss promotes obesity and metabolic issues in mice. Rsk4 is crucial for fibroblast growth factor-19 to regulate body weight.

Area of Science:

  • Neuroendocrinology
  • Metabolic research
  • Obesity studies

Background:

  • Ribosomal S6 kinase 4 (Rsk4) is primarily found in hypothalamic neurons.
  • Rsk4's role in energy homeostasis was previously considered negligible.
  • Understanding Rsk4's function is key to metabolic disease research.

Purpose of the Study:

  • To investigate the role of Rsk4 in energy homeostasis and diet-induced obesity.
  • To determine if Rsk4 influences the efficacy of fibroblast growth factor-19 (FGF19) signaling.
  • To explore Rsk4 as a potential therapeutic target for obesity.

Main Methods:

  • Utilized mouse models with Rsk4 deficiency.
  • Administered high-fat diets to induce obesity.
  • Assessed metabolic parameters and body weight changes.

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  • Investigated FGF19 signaling pathways in the hypothalamus.

    • Main Results:

    • Loss of Rsk4 did not impair basal energy homeostasis but exacerbated diet-induced obesity.
    • Rsk4 deficiency led to related metabolic disorders.
    • Rsk4 is essential for central FGF19 to reduce body weight in obese mice.

    Conclusions:

    • Rsk4 plays a critical role in preventing diet-induced obesity.
    • Rsk4 mediates the body weight-reducing effects of central FGF19.
    • Targeting Rsk4 may offer a novel strategy for obesity treatment.