The largest nationwide Polish study on migraine and sleep, involving 5,311 adults, found a strong association between migraine and poorer sleep quality. Nearly two-thirds (64.1%) of people with migraine reported poor sleep, compared with 38.7% of participants without headaches. People with migraine experienced problems across all assessed aspects of sleep, including falling asleep, sleep duration and efficiency, nighttime awakenings, and daytime functioning.

Poorer sleep was also associated with a greater migraine burden, including more frequent attacks, greater disability, higher stress and anxiety, and lower quality of life. The study additionally found that people with migraine were more likely to have a later chronotype, although the relationship between chronotype and migraine severity was weak.

The findings support a bidirectional relationship between migraine and sleep disturbances and suggest that sleep assessment should be routinely included in migraine care. However, because the study was cross-sectional and relied on self-reported data, it cannot establish causality. Further longitudinal studies using objective sleep measurements are needed.

Over nearly five decades, biomolecular simulation techniques have become indispensable tools for uncovering fundamental principles governing life at molecular scale. These computational approaches enable quantitative characterization of complex biomolecular events including protein folding, conformational dynamics and protein‑protein interactions, and have greatly advanced both fundamental and applied biological research. In recent years, the integration of machine learning, especially deep‑learning algorithms, has sparked substantial innovation within this field.

Glucagon-like peptide-1 (GLP-1) is secreted by intestinal L cells in response to postprandial glucose, yet how glucose triggers this secretion has remained unclear. Here, the authors show that glucose itself acts as a ligand for glucokinase (GK), independent of its metabolism. Glucose-bound GK directly interacts with and inhibits K_ATP channels, leading to membrane depolarization and GLP-1 release without any increase in intracellular ATP. This mechanism is distinct from the classical ATP-dependent model and is validated by GK mutations found in MODY2 patients. The study also reveals that SGLT1 mediates basal GLP-1 secretion at low glucose, while the GK-K_ATP axis drives the postprandial response at high glucose. These findings redefine glucose as a signaling molecule and GK as its receptor, offering new therapeutic avenues for diabetes and obesity.