Overview

• Two back-to-back Science papers confirmed that conserved noncoding elements tied to hibernation in mammals are present in human DNA
• Comparative genomics pinpointed switches near the FTO obesity locus whose alteration in mice adjusts weight gain, metabolic rate and body-temperature recovery
• Functional assays in mouse models demonstrated that mutating specific hibernator-associated elements fine-tunes gene hubs to accelerate or decelerate metabolism and thermoregulation
• Analysis revealed that most hibernator-linked genomic changes disable existing regulatory functions rather than create new ones, suggesting loss of constraints drives extreme metabolic flexibility
• University of Utah researchers are advancing the ‘genomic brakes’ hypothesis and evaluating these regulatory hubs as potential drug targets for metabolic and neuroprotective treatments