Research
Molecular
In insulin-resistant muscle, insulin fails to phosphorylate Akt or FoxO1, resulting in the inability to repress PGC-1alpha expression.
Understanding the failure of insulin action in insulin-resistant states can inform treatment strategies.
StrongSupportsmedium confidence
In contrast, in muscle taken from insulin resistant humans or in palmitate-treated insulin resistant myotubes, neither Akt nor FoxO1 was phosphorylated by insulin, resulting in a failure for nuclear exclusion of FoxO1 total protein.
Why this rating
The study includes direct observations from human muscle samples.
Source
PGC‐1α gene expression is down‐regulated by Akt‐mediated phosphorylation and nuclear exclusion of FoxO1 in insulin‐stimulated skeletal muscle
Robert J. Southgate et al. · The FASEB Journal · 2005
DOI 10.1096/fj.05-3993fje
otherCited 73×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Insulin phosphorylates Akt and FoxO1, leading to reduced nuclear abundance of FoxO1 and repression of PGC-1alpha mRNA expression in healthy skeletal muscle.Strong
- Insulin decreases the expression of genes involved in oxidative metabolism in healthy muscle through reduced FoxO1 phosphorylation and nuclear exclusion.Strong
Related findings · Molecular
- QRISK decreased markedly after weight loss from 18.9 ± 2.2% to 11.2 ± 1.6%, p < 0.0001.Strong
- Normalization of 10-year cardiovascular risk and heart age is possible after substantial dietary weight loss and remission of T2DM.Strong
- The Low-Fat Plus diet resulted in a greater reduction in total cholesterol compared to the Low-Fat diet, with changes of -0.46 mmol/L (-17.6 mg/dL) versus -0.24 mmol/L (-9.2 mg/dL) respectively (P = 0.01).Strong
This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →