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Muscle plasticity is influenced by renal function and caloric intake through the FGF23-vitamin D axis
Luz M Acevedo1,2, Ángela Vidal3, Escolástico Aguilera-Tejero3
1Department of Comparative Anatomy and Pathological Anatomy and Toxicology, Faculty of Veterinary Sciences, Laboratory of Muscular Biopathology, University of Cordoba, Spain.
Kidney function and obesity impact skeletal muscle plasticity by altering vitamin D levels. This review explores the kidney-bone-muscle axis
Area of Science:
- Endocrinology
- Nephrology
- Muscle Physiology
Background:
- Skeletal muscle plasticity is crucial for vertebrate metabolism.
- Renal dysfunction and obesity are prevalent conditions linked to skeletal muscle alterations.
- The interplay between kidney, bone, and muscle health significantly impacts patient quality of life.
Purpose of the Study:
- To review the influence of the kidney-bone-muscle axis on skeletal muscle plasticity.
- To elucidate the role of vitamin D and FGF23 in this axis.
- To connect renal dysfunction and obesity to muscle anabolism via this axis.
Main Methods:
- Literature review of existing studies.
- Analysis of the non-traditional kidney-bone-muscle axis.
- Examination of hormonal regulation involving vitamin D and FGF23.
Main Results:
- Renal disease reduces active vitamin D (1,25(OH)2-vitamin D) due to decreased renal mass and phosphate retention.
- Phosphate retention stimulates FGF23, which further inhibits vitamin D synthesis.
- Obesity increases FGF23 and decreases vitamin D, while caloric restriction has the opposite effect.
Conclusions:
- Phosphate retention and caloric intake modulate 1,25(OH)2-vitamin D levels.
- 1,25(OH)2-vitamin D plays a key role in skeletal muscle anabolism.
- Understanding this axis is vital for managing patients with renal dysfunction and obesity.
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