Overview

• University of Michigan researchers report in Molecular Metabolism that VMHCckbr neurons in the ventromedial hypothalamus support routine glucose control.
• The cells act during the first hours of sleep to prevent overnight hypoglycemia by promoting fat breakdown that supplies gluconeogenic fuel.
• Mice with optogenetically activated VMHCckbr neurons showed higher systemic glycerol, whereas chronic silencing disrupted nocturnal glycemia on continuous monitoring.
• The pathway depends on β3‑adrenergic signaling and increases glycerol availability without depleting hepatic glycogen or boosting hepatic gluconeogenic gene expression.
• The team proposes that overactivity of these neurons may relate to elevated nocturnal lipolysis and glucose in prediabetes, a hypothesis that has not yet been tested in humans.