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Microglia rely on mitochondrial complex I during development, suggesting that complex I deficiency in microglia may have a role in primary mitochondrial diseases.
Microglia rely on mitochondrial respiration to respond to demyelinating injury. However, mitochondrial respiration is not required to support microglial proliferation.
The intestinal symbiont Desulfovibrio, which is enriched in individuals with metabolic syndrome, is found to suppress the production of GLP-1 in male mice. The over-the-counter drug bismuth subsalicylate inhibits the effect of Desulfovibrio and restores GLP-1 levels.
Lecoutre, Maqdasy and Rizo-Roca show that whole-body pharmacological inhibition or adipocyte-specific deletion of glutaminase in mice activates thermogenesis in inguinal adipocytes and promotes metabolic health. They also link decreased plasma and adipose tissue glutamine-to-glutamate ratios to insulin resistance in humans with obesity.
Allaband et al. analyse how timing of sample collection affects the conclusions that can be drawn from microbiome studies, which has implications for study design.
The sphingosine-1-phosphate receptor 1 mediates the inhibitory effect of eicosapentaenoic acid on endothelial activation and atherogenesis, furthering our understanding of the cardioprotective role of omega-3 polyunsaturated fatty acids.
Fu, Mackowiak et al. show that cooperative action of the liver and the gut, rather than the liver alone, drives acetaldehyde clearance after alcohol consumption and modulates drinking behaviour.
Molecular pharmacological characterization and association testing of human GIPR genetic variants with follow-up analysis in mice shows that β-arrestins regulate GIPR signalling and thereby strongly contribute to metabolic outcomes.
The LITMUS consortium provides a resource of rodent MASLD models benchmarked against metabolic, histologic and transcriptomic features that are relevant for human MASLD. The work is useful for selecting relevant rodent models for studying this common disease.
Sekine et al. show that macrophages utilize different pathways to sense acute and chronic hypoxia, the latter relying preferentially on PNPO–PLP rather than hypoxia-inducible factors.
The transcriptional coregulators YAP/TAZ are shown to directly control leptin gene transcription, thereby uncoupling adipose tissue mass from leptin levels.
Exercise during the early active phase leads to more robust bone growth and maturation in young mice, through a mechanism dependent on oxidative phosphorylation.
Jiménez-Blasco et al. show that neurons exhibit moderately low glycolytic rates despite their activity being mainly supported by glucose to preserve redox balance.
Tan et al. identify a regulatory network between colonic EECs and the gut microbiota that controls l-glutamic acid production, appetite and body weight in mice.
Upon nutrient stress in hepatocellular carcinoma, the glycolytic enzyme PFKL facilitates mitochondria tethering to lipid droplets to engage lipid mobilization and ensure nutrient supply.
The metabolite agmatine derived from the gut microbiota contributes to a polycystic ovary syndrome-like phenotype in female mice and inhibits the secretion of glucagon-like peptide-1, thereby contributing to metabolic and ovarian dysfunction.
