TLCL deficiency reduces OXPHOS efficiency.
Newswise —
Regaining weight is a prevalent issue among individuals who have lost weight. Several research studies indicate that overweight individuals experience a decrease in overall energy expenditure after shedding pounds. This decline in energy expenditure disproportionately affects different tissues, resulting in an energetic mismatch. This imbalance is primarily due to a reduction in lean tissue, thereby increasing the likelihood of regaining weight. Despite identifying this phenomenon, the precise mechanisms of how weight loss affects skeletal muscle mitochondrial respiration remain unknown, and concrete evidence is yet to be established.
In April 2023, Life Metabolism featured a study by Professor Katsuhiko Funai at the University of Utah titled "Weight loss elevates skeletal muscle mitochondrial energy efficiency in obese mice." The research team discovered that obese mice undergoing weight loss experienced an improvement in the efficiency of skeletal muscle mitochondrial oxidative phosphorylation, leading to decreased energy expenditure throughout the body. This reduction in energy expenditure may contribute to weight regain following weight loss.
To investigate the effects of weight loss on mitochondrial energy metabolism, researchers conducted a study using obese mice treated with dietary interventions to induce weight loss. High-resolution respirometry and fluorometry measurements were used to assess changes in mitochondrial energy metabolism, while mitochondrial proteomes and lipidomes were analyzed to examine any related changes. The results showed that while there was no significant change in mitochondrial proteomes or respiratory chain supercomplex formation, weight loss did lead to an increase in oxidative phosphorylation efficiency (as seen in Figure 1). Additionally, the researchers found that weight loss accelerated the remodeling of mitochondrial cardiolipin (CL) acyl-chains, resulting in an increase in the content of tetralinoleoyl CL (TLCL), a lipid species believed to be critical for respiratory enzymes. Knocking down the CL acyltransferase tafazzin was shown to reduce TLCL levels and skeletal muscle oxidative phosphorylation levels, allowing mice to avoid diet-induced weight gain (also shown in Figure 1). Taken together, these findings suggest that weight loss can increase skeletal muscle mitochondrial energy production efficiency, leading to a reduction in overall energy expenditure in the body.
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Reference: Patrick J Ferrara et al. (2023) Weight loss increases skeletal muscle mitochondrial energy efficiency in obese mice. Life Metabolism. https://academic.oup.com/lifemeta/advance-article/doi/10.1093/lifemeta/load014/7103241
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