Research

Hormonal

Mitochondrial dysfunction, characterized by impaired oxidative capacity and increased reactive oxygen species (ROS), promotes insulin resistance in skeletal muscle by causing the accumulation of lipotoxic lipid intermediates (diacylglycerol and ceramide) that inhibit insulin signaling.

For those with insulin resistance or T2DM, focusing on interventions that support mitochondrial health (like exercise which upregulates PGC-1α) may be more effective than focusing solely on caloric restriction. The paper suggests that boosting mitochondrial function can improve insulin sensitivity, potentially by reducing toxic lipid buildup in muscles.

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A decrease in metabolic substrate oxidation appears as a primary defect, which, by triggering a cascade of events culminating with the intracellular accumulation of the diacylglycerol and ceramide, hampers insulin signalling and promotes insulin resistance.
Domenico Sergi et al. · Frontiers in Physiology · 2019

Why this rating

The paper reviews extensive human and animal studies, including microarray data and in vivo assessments, though noting conflicting evidence.

Source

Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet

Domenico Sergi et al. · Frontiers in Physiology · 2019

DOI 10.3389/fphys.2019.00532

narrative_reviewCited 339×
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DOI resolved against Crossref · corpus check 2026-06-10

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