Koss, A. | bioRxiv Science

bioRxiv2026

Recurring daytime and nighttime modes of VOC emissions in a cool-temperate oak forest

Plants emit substantial amounts of biogenic volatile organic compounds (VOCs) that link plant physiological activity to ecological interactions and atmospheric chemistry. However, the processes regulating VOC emissions within the forest air and at the interface directly above the canopy remain poorly characterized. In this study, we investigated forest-scale VOC dynamics in a cool-temperate deciduous forest dominated by Quercus crispula using high-time- and high-mass-resolution proton-transfer-reaction time-of-flight mass spectrometry (PTR-ToF-MS) integrated with positive matrix factorization (PMF). This non-targeted, process-oriented framework was applied to forest-interior and canopy-top atmospheres during rain-free summer days in 2024 and 2025 to extract dominant modes of VOC emissions. The PMF consistently resolved two recurring modes characterized by the daytime and nighttime enhancement patterns. The daytime mode was dominated by isoprene and its oxidation products and demonstrated strong light- and temperature-dependence, whereas the nighttime mode was enriched in mono- and sesquiterpenes. The daytime contribution exhibited a pronounced morning-afternoon asymmetry, indicating non-linear physiological and canopy-scale controls. These patterns were reproducible across the years. This study demonstrates that combining PTR-ToF-MS with PMF enables robust, top-down identification of recurring modes of forest VOC variability within and above forest canopies, linking leaf-level physiology and ecosystem-scale atmospheric exchange. HighlightForest-scale VOC emissions were resolved into recurring daytime and nighttime modes using a non-targeted PTR-ToF-MS and PMF framework.

physiology↗

bioRxiv2025

Metformin inhibits mitochondrial complex I in intestinal epithelium to promote glycemic control

Metformin is a therapeutically versatile biguanide drug primarily prescribed for type II diabetes. Despite its extensive use, the mechanisms underlying many of its clinical effects, including attenuated postprandial glucose excursions, elevated intestinal glucose uptake, and increased production of lactate, Lac-Phe and GDF15, remain unclear. Here, we map these and other clinical effects of metformin to intestine-specific mitochondrial complex I inhibition. Using human metabolomic data and an orthogonal genetics approach in male mice, we demonstrate that metformin suppresses citrulline synthesis, a metabolite generated exclusively by small intestine mitochondria, and increases GDF15 by inhibiting the mitochondrial respiratory chain at complex I. This inhibition co-opts the intestines to function as a glucose sink, driving uptake of excess glucose and converting it to lactate and Lac-Phe. Notably, the glucose-lowering effect of another biguanide, phenformin, and berberine, a structurally unrelated nutraceutical, similarly depends on intestine-specific mitochondrial complex I inhibition, underscoring a shared therapeutic mechanism.

physiology↗