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) ”

Ineke Luijten, Ami Onishi, Eleanor J. McKay, Tore Bengtsson, Robert K. Semple

Pik3r1 insulin resistance Ucp1 thermogenesis metabolic syndrome

TLDR Increased energy use in Pik3r1-related insulin resistance isn't due to Ucp1 thermogenesis.

The study investigates the mechanism behind increased energy expenditure in Pik3r1-related insulin resistance, which is not explained by Ucp1-mediated thermogenesis. Pik3r1Y657* mice, which mimic human SHORT syndrome, show increased energy expenditure and reduced metabolic efficiency without changes in food intake, physical activity, or Ucp1-dependent thermogenesis. The research suggests that the protective energy expenditure in these mice is due to an alternative metabolic process rather than Ucp1-mediated BAT hyperactivation or impaired thermal insulation. Further studies are needed to explore other potential mechanisms, such as non-Ucp1-mediated futile cycling, to understand how these mice and humans are protected from lipotoxicity despite insulin resistance.

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