All articles tagged with #sf1 neurons
New Neuron-based research shows SF1 neurons in the ventromedial hypothalamus stay active after exercise and are needed for endurance gains; blocking these neurons post-workout prevents improvements, suggesting brain activity after exercise helps the body adapt and use energy more efficiently—potential implications for aging, stroke recovery, and athletic performance.
A UT Southwestern study shows SF1-producing neurons in the ventromedial hypothalamus encode a memory of exercise that programs and boosts endurance and metabolic benefits. Blocking these neurons prevents endurance gains, while stimulating them after training pushes past typical plateaus, suggesting the brain acts as a central mediator in exercise adaptation and offering potential therapies to simulate exercise for those with limited mobility.
New research shows metformin can act in the brain, reaching the ventromedial hypothalamus and inhibiting Rap1 signaling in SF1 neurons to help regulate glucose in mice, a mechanism distinct from its liver and gut effects. When Rap1 was removed, metformin no longer helped diabetes-like symptoms, suggesting a brain pathway. This could lead to brain-targeted diabetes therapies and broaden metformin’s uses, though human studies are needed and side effects like GI distress and kidney risk remain concerns; the drug is also linked to aging benefits.
A Neuron study in mice shows that endurance gains from repeated workouts rely on brain changes after exercise, specifically SF1 neurons in the ventromedial hypothalamus that stay active for at least an hour post-exercise; training enhances SF1 activity and the number of activated neurons, and blocking these neurons or silencing them after exercise abolishes endurance gains, indicating post-exercise brain activity is crucial for long-term adaptation and could inform strategies to help aging or mobility-impaired individuals stay active.