The Metabolically Protective Energy Expenditure Increase of Pik3r1-Related Insulin Resistance Is Not Explained by Ucp1-Mediated Thermogenesis
February 2024
in “
bioRxiv (Cold Spring Harbor Laboratory)
”
Preprint — not peer reviewed. This was posted to a preprint server or data repository. It has not been through a journal's review process, and its findings may change or not hold up.
Studysummary This study found that Pik3r1 Y657* mice, which model human SHORT syndrome, show increased energy expenditure despite insulin resistance, but this is not due to changes in locomotion, thermoregulation, or Ucp1-dependent thermogenesis, suggesting a different metabolic mechanism may protect against lipotoxicity.
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