Research
Macro partitioning
Insulin-resistant skeletal muscle exhibits significantly lower abundance of Carnitine Palmitoyltransferase 1B (CPT1B) and specific Complex I subunits, which may contribute to lipid accumulation.
Obese, insulin-resistant individuals have less of the protein (CPT1B) that shuttles fat into mitochondria for burning. This bottleneck may cause fat to accumulate in the muscle, worsening insulin resistance.
GoodSupportsHIGH confidence
Tandem mass spectrometry identified protein abundance differences... including lower abundance of complex I subunits and... carnitine palmitoyltransferase 1B... might contribute to the accumulation of lipid and BCAA frequently associated with the pathogenesis of insulin resistance.
Why this rating
Proteomic analysis with validation via immunoblotting.
Source
Increased Reactive Oxygen Species Production and Lower Abundance of Complex I Subunits and Carnitine Palmitoyltransferase 1B Protein Despite Normal Mitochondrial Respiration in Insulin-Resistant Human Skeletal Muscle
Natalie Lefort et al. · Diabetes · 2010
DOI 10.2337/db10-0174
mechanism_only · n=34Cited 174×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- In obese, insulin-resistant individuals, skeletal muscle mitochondria exhibit increased reactive oxygen species (ROS) production and lower abundance of Complex I subunits and CPT1B protein, despite maintaining normal maximal mitochondrial respiration rates.Good
- Mitochondria from insulin-resistant muscle maintain higher thermodynamic driving forces (more negative static head ATP free energy) at low metabolic flux, which predicts higher ROS production.Good
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