Hormonal
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.
For obese, insulin-resistant individuals, the problem isn't that your mitochondria can't burn fat (maximal capacity is normal), but that they are leaking harmful ROS and have lower levels of key fat-burning entry proteins (CPT1B). This suggests focusing on strategies that reduce oxidative stress and improve mitochondrial efficiency rather than just 'boosting capacity'.
Rates of pyruvate and palmitoyl-DL-carnitine (both including malate) ROS production were significantly higher in obesity... NADH- and FADH2-linked maximal respiration rates were similar between lean and obese individuals... Tandem mass spectrometry identified protein abundance differences... including lower abundance of complex I subunits and... carnitine palmitoyltransferase 1B.
Why this rating
Direct measurements on isolated human mitochondria with matched controls, though observational in nature regarding the insulin resistance state.
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
More from this paper
- 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
- Insulin-resistant skeletal muscle exhibits significantly lower abundance of Carnitine Palmitoyltransferase 1B (CPT1B) and specific Complex I subunits, which may contribute to lipid accumulation.Good
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