Metabolic dysfunction in obesity is related to impaired suppression of fatty acid release from adipose tissue by insulin
Authors' conclusion
Insulin's ability to suppress FA release from aSAT in obesity is related to enhanced insulin-mediated glucose uptake and metabolic health in peripheral tissues.
Study context
- Population
- Adults with obesity (BMI = 34 [SD 3] kg/m²), assessed by hyperinsulinemic-euglycemic clamp, stable isotope kinetics, abdominal subcutaneous adipose tissue (aSAT) and skeletal muscle biopsies and MRI
- Participants
- 66 adults
- Comparison
- Low FA Ra suppression vs High FA Ra suppression
- Low FA Ra suppressionn = 8
- High FA Ra suppressionn = 8reference
- Outcome
- Relationships of insulin-mediated glucose uptake with clinical outcomes and deep-phenotyping measures, incl. FA Ra into the systemic circulation
Main finding
As reported in the abstract
Correlates of insulin-mediated FA Ra suppression
FA Ra suppression vs insulin-mediated glucose uptake
r = 0.51
p < 0.01
FA Ra suppression vs liver fat
r = −0.36
p < 0.01
FA Ra suppression vs visceral fat
r = −0.42
p < 0.01
Further findings
aSAT proteomics: extracellular matrix collagen protein
- Greater extracellular matrix collagen protein in low vs high FA Ra suppression
Skeletal muscle lipidomics: acyl-chain length (n = 18)
- FA Ra suppression vs acylcarnitine acyl-chain length
- r = −0.42; p = 0.02
- FA Ra suppression vs triacylglycerol acyl-chain length
- r = −0.51; p < 0.01
- Insulin-mediated glucose uptake vs acylcarnitine acyl-chain length
- r = −0.49; p < 0.01
- Insulin-mediated glucose uptake vs triacylglycerol acyl-chain length
- r = −0.40; p < 0.01
Original publication
Metabolic dysfunction in obesity is related to impaired suppression of fatty acid release from adipose tissue by insulin. Obesity (Silver Spring). Published 29 March 2023. doi:10.
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