Insulin Signaling Is Preserved in Skeletal Muscle During Early Diabetic Ketoacidosis
Authors' conclusion
DKA impairs insulin-stimulated activation of glycogen synthase, whereas insulin signal transduction to glucose transport and protein synthesis remains intact. Reversal of insulin resistance during treatment of DKA should target postreceptor mediators of glucose uptake.
Study context
- Population
- Patients with T1Dcrossover
- Participants
- 9 patients
- Comparison
- Total insulin withdrawal for 14 hours vs insulin-controlled euglycemia, each before a high-dose insulin clamp
Methodological detailscrossover
- Crossover
Primary result
As reported in the abstract
Insulin-stimulated dephosphorylation of glycogen synthase in skeletal muscle
- Decreased with insulin withdrawal vs control by ∼30% (P < .05)
- Insulin transduction to glucose transport and protein synthesis (Akt, AS160, mTOR, 4E-BP) intact
Further findings
Glucose oxidation
- Decreased during insulin withdrawal by ∼30% (P < .05)
Glucose transporter (GLUT4) and mitochondrial proteins (succinate dehydrogenase complex subunit A, prohibitin 1) expression
- Unaffected by the intervention
Original publication
Insulin Signaling Is Preserved in Skeletal Muscle During Early Diabetic Ketoacidosis. J Clin Endocrinol Metab. Published 9 August 2023. doi:10.
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