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Skelton, H. E.

Publications and source records attributed to Skelton, H. E..

2 recordsLinked to original sources

A Preoptic Neuronal Population Regulates Energy Expenditure and Balance

Maintaining energy balance requires coordination between food intake and energy expenditure, yet the neural pathways that regulate energy expenditure remain unclear. This study identifies kappa opioid receptor-expressing neurons in the preoptic area of the hypothalamus as a key regulator of whole-body metabolism. Using mouse models combined with fiber photometry, chemogenetic activation and inhibition, and chronic disruption of synaptic output, the results show that activity of these neurons follows daily pattern, are suppressed during feeding, and their inhibition acutely increases energy expenditure, body temperature, and activity levels. Long-term inhibition of this population produces sustained weight loss, selective reduction of white fat, preservation of lean mass and brown fat, and improved glucose tolerance even during high-fat feeding. These findings reveal a previously unrecognized circuit that links metabolic state with daily timing cues and suggest that targeting this neuronal population may offer new strategies for treating obesity and related metabolic disorders.

neuroscience↗

Preoptic activation induces a torpor-like hypothermic and hypometabolic state that is cerebroprotective

Therapeutic hypothermia for stroke has been limited by shivering, increased metabolic demand, and poor patient tolerance. Engaging endogenous thermoregulatory circuits to lower body temperature may overcome these limitations and modulate metabolism, offering an integrated approach to cerebroprotection. Here, we show that chemogenetic activation of neurons in the preoptic area (POA) elicits a torpor-like state in mice, characterized by sustained hypothermia and hypometabolism. In an animal stroke model, this endogenous hypothermic state significantly reduced infarct volume and improved motor outcomes compared to controls, whereas maintaining normothermia attenuated these protective effects. To explore metabolic mechanisms contributing to this state, we performed untargeted metabolomic profiling 30 minutes after POA activation and identified coordinated shifts in nucleotide, phospholipid, and sphingolipid pathways. These rapid, temperature-dependent changes indicate a metabolically reprogrammed state that may enhance neuronal resilience during ischemic stress. Together, our findings suggest that POA-driven hypothermia confers cerebroprotection through specific metabolic adaptations with translational potential.

neuroscience↗