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Ucp1 Ablation Improves Skeletal Muscle Glycolytic Function in Aging Mice
Jin Qiu1, Yuhan Guo1, Xiaozhen Guo2
1Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|November 21, 2024
Summary
Aging impairs brown fat function, but creatine metabolism in other fat tissues and muscles may sustain energy balance. This study reveals how creatine transport between tissues compensates for aging-related metabolic decline.
Area of Science:
- Metabolic research
- Aging biology
- Adipose tissue and muscle physiology
Background:
- Aging is associated with declining organ function, particularly thermogenic adipose tissue (BAT).
- The interplay between adipose tissue and muscle during aging is not well understood.
- Defective BAT function precedes other age-related functional declines.
Purpose of the Study:
- To investigate the crosstalk between adipose tissue and muscle in aging.
- To understand the compensatory mechanisms for declined BAT function during aging.
- To explore the role of creatine metabolism in metabolic homeostasis during aging.
Main Methods:
- Utilized UCP1 knockout (KO) mice and wild-type (WT) littermates for comparative analysis.
- Performed RNA-sequencing and metabolomic analysis on adipose tissue and muscle.
- Employed metabolite tracing and molecular analysis to investigate creatine biosynthesis and uptake.
- Used creatine analog β-GPA and UCP1 inhibitor α-CD to assess functional impacts.
Main Results:
- UCP1 KO mice showed impaired BAT function but maintained glucose homeostasis and increased energy expenditure.
- Increased creatine levels were observed in inguinal adipose tissue (iWAT) and muscle of UCP1 KO mice.
- Evidence suggests increased creatine biosynthesis in iWAT and uptake in muscle, indicating iWAT-to-muscle creatine transport.
- β-GPA treatment normalized muscle function differences, while α-CD improved muscle glycolytic function and glucose metabolism in aging mice.
Conclusions:
- Inguinal adipose tissue and skeletal muscle can compensate for declining brown adipose tissue function in aging.
- Creatine metabolism plays a crucial role in maintaining metabolic homeostasis during aging.
- Targeting creatine metabolism may offer therapeutic strategies for age-related metabolic dysfunction.
