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Background <p>Metabolic dysfunction–associated steatotic liver disease (MASLD) is closely linked to obesity, insulin resistance, and endocrine dysregulation. Although calorie restriction is widely used for metabolic control, it is often accompanied by unintended skeletal muscle loss, which may negatively affect long-term metabolic outcomes. Therefore, identifying a dietary strategy that improves metabolic health while preserving muscle mass is of clinical importance.</p> Methods <p>This study combined retrospective clinical observations with an in vivo high-fat diet (HFD)-induced obese mouse model to evaluate the effects of low-calorie balanced diet (LCD). Clinical data were used to assess changes in metabolic parameters and body composition. In parallel, obese mice subjected to LCD intervention were evaluated for body weight, glucose metabolism, hepatic steatosis, and skeletal muscle morphology. Gene expression related to hepatic lipid metabolism and muscle atrophy was analyzed.</p> Results <p>LCD intervention improved metabolic parameters, reduced body weight gain, and alleviated hepatic lipid accumulation in both clinical observations and the animal model. In HFD-fed mice, LCD improved glucose homeostasis and partially reversed hepatic steatosis. Importantly, skeletal muscle structure was preserved, and the expression of muscle atrophy–related genes, including MSTN, FOXO3a, and MuRF1, was reduced. In the liver, LCD decreased the expression of lipogenic genes such as SREBP-1c, FASN, and ACC, while partially restoring fatty acid oxidation–related genes including PPARα and CPT1α.</p> Conclusion <p>LCD improves metabolic dysfunction and hepatic steatosis while preserving skeletal muscle integrity in obesity. These findings provide translational evidence supporting LCD as a practical dietary strategy for MASLD management and highlight the importance of coordinated metabolic regulation between liver and skeletal muscle.</p> Graphical abstract <p></p>

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A low-calorie balanced diet improves hepatic steatosis and preserves skeletal muscle in obesity: evidence from clinical and experimental studies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月4日

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  • Ruijia Li,
  • Zheng Yang,
  • Yingyi Chen,
  • Yanju Li,
  • Haoyuan Xu,
  • Zhiyong Rao

摘要

Background

Metabolic dysfunction–associated steatotic liver disease (MASLD) is closely linked to obesity, insulin resistance, and endocrine dysregulation. Although calorie restriction is widely used for metabolic control, it is often accompanied by unintended skeletal muscle loss, which may negatively affect long-term metabolic outcomes. Therefore, identifying a dietary strategy that improves metabolic health while preserving muscle mass is of clinical importance.

Methods

This study combined retrospective clinical observations with an in vivo high-fat diet (HFD)-induced obese mouse model to evaluate the effects of low-calorie balanced diet (LCD). Clinical data were used to assess changes in metabolic parameters and body composition. In parallel, obese mice subjected to LCD intervention were evaluated for body weight, glucose metabolism, hepatic steatosis, and skeletal muscle morphology. Gene expression related to hepatic lipid metabolism and muscle atrophy was analyzed.

Results

LCD intervention improved metabolic parameters, reduced body weight gain, and alleviated hepatic lipid accumulation in both clinical observations and the animal model. In HFD-fed mice, LCD improved glucose homeostasis and partially reversed hepatic steatosis. Importantly, skeletal muscle structure was preserved, and the expression of muscle atrophy–related genes, including MSTN, FOXO3a, and MuRF1, was reduced. In the liver, LCD decreased the expression of lipogenic genes such as SREBP-1c, FASN, and ACC, while partially restoring fatty acid oxidation–related genes including PPARα and CPT1α.

Conclusion

LCD improves metabolic dysfunction and hepatic steatosis while preserving skeletal muscle integrity in obesity. These findings provide translational evidence supporting LCD as a practical dietary strategy for MASLD management and highlight the importance of coordinated metabolic regulation between liver and skeletal muscle.

Graphical abstract