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Optimization of energy and carbon–nitrogen allocation maximizes the proliferation and functionality of chimeric antigen receptor (CAR)-T cells. Lakhani et al. report that tonic signalling elements (scFvs) affect CAR-T cell metabolic fitness in an antigen-independent manner. A modest carbon–nitrogen emission (overflow) and resilient metabolic phenotype (compatibility) are associated with effective CAR-T cell therapy.
Lakhani et al. offer insight into the metabolic reconfigurations driven in T cells by chimeric antigen receptors (CARs) that differ only in their extracellular domains.
In this issue of Nature Metabolism, the research team of Mitchell Lazar reveals unexpected consequences of double loss of the coregulators NCOR1 and NCOR2 (NCOR1/2) in hepatocytes of adult mice, which affects chromatin functioning and glucocorticoid receptor (GR)-mediated gene transcription.
Hauck et al. show that during fasting, nuclear receptor corepressors 1 and 2 act together to activate the transcription of target genes, which is critical for the physiological response to fasting in mice.
A new engineering strategy for improving the biosynthesis of secondary metabolites in Streptomyces has been developed through the analysis of genes co-evolved with biosynthetic gene clusters. This strategy has been verified in 11 Streptomyces strains to enhance production of 16,385 metabolites, showing potential applications in drug discovery and industrial production.
The authors develop a metabolic engineering strategy for improving polyketide production of industrial interest and discovering new natural products in bacteria.
Thiazolidinediones (TZDs) are potent insulin-sensitizing drugs, but their use is accompanied by adverse side-effects. Rohm et al. now report that TZD-stimulated macrophages release miR-690-containing vesicles that improve insulin sensitization and bypass unwanted side-effects.
Recent technological advances permit the profiling of metabolic changes in single cells, which sheds light on how metabolism regulates immune responses. We advocate for accessible and standardized tools to reduce the barrier of entry to immunometabolism studies and facilitate the translation of fundamental findings towards clinical applications.
Rohm et al. show that small extracellular vesicles from adipose tissue macrophages from obese rosiglitazone-treated mice ameliorate glucose tolerance and insulin sensitivity in obese mice, while circumventing the adverse effects of rosiglitazone.
Kim et al. discover a subset of neurons that innervate the Drosophila intestine and act as postprandial taste-independent sensors for sodium, directing a behavioural preference for sodium following salt deprivation.
Klingelhuber, Frendo-Cumbo et al. develop a proteomic atlas elucidating the intracellular spatiotemporal changes in protein levels and localizations during human adipogenesis.
Maternal circadian rhythms influence the health of infants. Cui, Xu and colleagues find that disruption of maternal rhythms impairs neonatal immune cell function and aggravates neonatal inflammatory disorders, which can be rescued by the administration of docosahexaenoic acid (a metabolite found in breast milk).
In mice, disruption of circadian rhythms during pregnancy aggravates neonatal inflammation via metabolic reprograming of myeloid cells in the offspring.
A new sensor that detects optoacoustic signals generated by mid-infrared light enables measurement of glucose concentration from intracutaneous tissue rich in blood. This technology does not rely on glucose measurements in interstitial fluid or blood sampling and might yield the next generation of non-invasive glucose-sensing devices for improved diabetes management.
A new methodology uses intravital time-gated mid-infrared optoacoustic signals for accurate non-invasive measurements of glucose concentrations in blood-rich volumes of the skin.
AMPK directly phosphorylates the mitochondrial protein SYNJ2BP to facilitate its interaction with the RNA-binding protein SYNJ2a, which transports Pink1 mRNA into neurites. AMPK inhibition downstream of insulin signalling untethers Pink1 mRNA from neuronal mitochondria and favours PINK1-dependent mitophagy in neurons. ApoE4-induced insulin receptor internalization reverses the process by stabilizing Pink1 mRNA binding to neuronal mitochondria.
When preparing your manuscript, clear presentation of the data and concise writing are key. In this Editorial, we offer tips on how to better communicate your results.
Hees et al. identify a mechanism that integrates insulin signalling with distal mitochondrial quality control in neurons via AMPK/PINK1, with implications for mitochondrial dysfunction in the context of insulin resistance in neurons.