Yuzefovych · American journal of physiology. Endocrinology and metabolism 2010 · in vitro controlled cell culture experiment · n=?

Different effects of oleate vs. palmitate on mitochondrial function, apoptosis, and insulin signaling in L6 skeletal muscle cells: role of oxidative stress.

Cited 284 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

In vitro cell culture study without human clinical data

PubMed 20876761 · doi:10.1152/ajpendo.00238.2010 · record verified 2026-08-29

What was done

Researchers evaluated the comparative effects of the saturated fatty acid palmitate, the unsaturated fatty acid oleate, and their combination in cultured L6 skeletal muscle cells. They assessed mitochondrial reactive oxygen species (mtROS) production, mitochondrial DNA (mtDNA) damage, mitochondrial function (ATP levels, PGC-1α, TFAM), JNK activation, apoptosis, and insulin signaling (Akt Ser473 phosphorylation), as well as the impact of blocking ceramide synthesis and adding the antioxidant N-acetylcysteine (NAC).

What was found

No numerical values or effect sizes were reported in the abstract (aside from a threshold concentration of palmitate ≥0.5 mM). Palmitate significantly increased mtROS production, mtDNA damage, JNK induction, apoptosis, and inhibited insulin signaling, while decreasing PGC-1α and TFAM expression. Blocking ceramide synthesis abolished palmitate's effects on mtROS, viability, and insulin signaling. Oleate alone caused no mtROS generation or mtDNA damage; when combined with palmitate, oleate prevented mtDNA damage, apoptosis, and Akt inhibition, while increasing ATP levels, viability, and PGC-1α expression. NAC restored PGC-1α and TFAM expression during palmitate exposure.

Why it matters

This study highlights contrasting cellular mechanisms of saturated versus unsaturated fatty acids in muscle cells, indicating that palmitate impairs insulin signaling via ceramide- and mtROS-driven mitochondrial dysfunction, while oleate exerts a protective counter-effect.

Limits

All findings are derived from an in vitro rat skeletal muscle cell line (L6), precluding direct translation to human physiology or in vivo metabolism. The abstract provides no quantitative data, error ranges, or replicate counts (n).

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