Beta2-agonist Impairs Muscle Insulin Sensitivity in Persons With Insulin Resistance
Authors' conclusion
Our findings suggest that beta2-agonist inhibits glycogenesis, whereas intralipid inhibits glycolysis in skeletal muscle of insulin-resistant individuals. These results should be addressed in future treatment of insulin resistance with beta2-agonist.
Study context
- Population
- Insulin-resistant, overweight subjectscrossover
- Participants
- 10 participants
- Comparison
- Beta2-agonist vs no beta2-agonist during hyperinsulinemic isoglycemic clamp, with and without intralipid infusion
- Outcome
- Insulin-stimulated muscle glucose uptake
- Follow-up
- 3-hour hyperinsulinemic isoglycemic clamp
Methodological detailscrossover, Beta2-agonist infused 2 hours into the clamp; muscle biopsies before, at 2 hours and at end of clamp, analysed by metabolomics and lipidomics
- Crossover
- Beta2-agonist infused 2 hours into the clamp; muscle biopsies before, at 2 hours and at end of clamp, analysed by metabolomics and lipidomics
Main finding
As reported in the abstract
- Beta2-agonist, independently from and additively to intralipid, impairs insulin-stimulated muscle glucose uptake via different mechanisms
- Beta2-agonist plus intralipid nearly eliminates insulin-dependent muscle glucose uptake
- Both beta2-agonist and intralipid elevated muscle glucose-6-phosphate
- Only intralipid caused accumulation of downstream muscle glycolytic intermediates
- Beta2-agonist attenuated incorporation of glucose into glycogen
Original publication
Beta2-agonist Impairs Muscle Insulin Sensitivity in Persons With Insulin Resistance. J Clin Endocrinol Metab. Published 31 May 2024. doi:10.
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