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Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

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Mitochondrial function and dysfunction in exercise and insulin resistance.

Graham P Holloway¹

¹Department of Human Health & Nutritional Sciences, University of Guelph, Guelph, ON N1G 2W1, Canada. ghollowa@uoguelph.ca

Applied Physiology, Nutrition, and Metabolism = Physiologie Appliquee, Nutrition Et Metabolisme

|May 19, 2009

Summary

This summary is machine-generated.

Fatty acid translocase (FAT/CD36) regulates fatty acid metabolism in skeletal muscle. Increased FAT/CD36 transport, not impaired oxidation, drives lipid accumulation and insulin resistance.

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Published on: January 23, 2018

Area of Science:

Skeletal Muscle Physiology
Metabolic Regulation
Insulin Resistance Research

Background:

Fatty acid translocase (FAT/CD36) plays a key role in regulating fatty acid metabolism in skeletal muscle.
Previous models linked reduced fatty acid oxidation to insulin resistance via lipid accumulation.
Emerging evidence suggests a more complex interplay between fatty acid transport and oxidation.

Purpose of the Study:

To investigate the role of FAT/CD36 in coordinating fatty acid transport and oxidation during exercise.
To explore the contribution of FAT/CD36-mediated fatty acid uptake versus mitochondrial oxidation in the development of insulin resistance.
To challenge the existing paradigm by proposing an alternative model for lipid accumulation in insulin-resistant skeletal muscle.

Main Methods:

Subcellular redistribution analysis of FAT/CD36 during exercise.
Assessment of mitochondrial content and fatty acid oxidation capacity in skeletal muscle.
Quantification of long-chain fatty acid (LCFA) transport rates.
Comparison of lipid accumulation in insulin-resistant versus healthy muscle models.

Main Results:

Exercise induces subcellular redistribution of FAT/CD36, enhancing both plasma membrane fatty acid transport and mitochondrial oxidation.
In some insulin-resistant muscles, both mitochondrial content and fatty acid oxidation are elevated.
Despite increased oxidation, these muscles accumulate lipids due to a disproportionately greater increase in fatty acid transport.
A permanent sarcolemmal redistribution of FAT/CD36 leads to increased LCFA transport rates.

Conclusions:

The balance between LCFA transport and oxidation, rather than solely oxidation capacity, is critical in determining insulin resistance.
Increased skeletal muscle lipid accumulation is primarily driven by an elevated rate of LCFA transport via FAT/CD36, exceeding oxidative capacity.
This revised model highlights FAT/CD36 as a central regulator in the pathogenesis of insulin resistance.