Research
Hormonal
Mitochondrial dysfunction in aging skeletal muscle, characterized by reduced oxidative capacity and increased ROS production, directly impairs insulin signaling and promotes insulin resistance.
Supporting mitochondrial health through regular physical activity is crucial for maintaining metabolic flexibility and insulin sensitivity as you age.
ModerateSupportsMEDIUM confidence
Mitochondrial dysfunction will cause an increase in ROS production, and high levels of ROS impair insulin signaling pathways and induce skeletal muscle insulin resistance.
Why this rating
Based on a review of mechanistic studies in humans and animals.
Source
Mechanism of increased risk of insulin resistance in aging skeletal muscle
Jian Shou et al. · Diabetology & Metabolic Syndrome · 2020
DOI 10.1186/s13098-020-0523-x
narrative_reviewCited 265×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Exercise acts as a non-pharmacological intervention that counteracts age-related insulin resistance by enhancing mitochondrial oxidative capacity, improving autophagy, and reducing oxidative stress and inflammation.Good
- Skeletal muscle aging independently increases the risk of insulin resistance through a convergence of mitochondrial dysfunction, intramyocellular lipid accumulation, chronic inflammation, oxidative stress, and sarcopenia.Moderate
- Intramyocellular lipid (IMCL) accumulation, specifically the buildup of ceramides and diacylglycerol (DAG), impairs insulin signaling by activating inflammatory pathways and interfering with Akt activity.Moderate
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