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Miller et al. use fast thermal preservation and mass spectrometry imaging to reveal rapid neuron-layer metabolic responses to stimulation within a brain slice. Stimulation increases glucose use and converts spent ATP into metabolic fuel, via inosine.
Lundgren et al. show that in response to transient cold exposure, a distinct subpopulation of brown adipocytes carries out a lipogenic response involving production of acylcarnitines, which enables an improved thermogenic response to secondary cold exposure.
This study presents a comprehensive pipeline to profile transmembrane receptors involved in macrophage-driven inflammation in pancreatic islets during the onset of diabetes. The authors identify GPR132 as a mediator of macrophage-driven inflammation and find compounds that reduce inflammation and improve glycaemic control.
The authors develop synthetic biotics, engineered from bacteria, that could treat phenylketonuria, an inherited defect of phenylalanine (Phe) metabolism.
Yao and Gong et al. identify WD40 repeat-containing protein 6 (WDR6) to be upregulated in the liver of insulin-resistant mice. WDR6 contributes to promoting hepatic de novo lipogenesis during insulin resistance by upregulation of fatty acid synthase, and the authors identify a small molecule to inhibit this effect of WDR6 and reduce hepatic steatosis.
In young women, brain insulin action enhances peripheral insulin sensitivity, but only during the follicular phase of the menstrual cycle. This effect is absent in the luteal phase, possibly due to hypothalamic insulin resistance.
Gao et al. perform functional profiling of 60 genetic variants of glucagon-like peptide 1 receptor (GLP1R) in vitro, and link variants with impaired GLP1R cell surface expression or cAMP activation to defective insulin secretion in vitro and to impaired glucose homeostasis and adiposity in the UK Biobank.
The authors explore the molecular signature of skeletal muscle adaptations to an acute bout of exercise in mice, providing a valuable resource that includes transcriptomic, epigenetic, proteomic and phosphoproteomic changes in muscle plasticity.
Longitudinal deep lipidome profiling reveals >800 lipid species, many of which are associated with health-to-disease transitions in diabetes, ageing and inflammation.
This study reports the mouse islet atlas, a curated resource integrating scRNA-seq data of over 300,000 cells from nine datasets, covering pancreas development, homeostasis and disease states.
TMEM164 is an early-response intrinsic factor that inhibits the induction of neurotoxic reactive astrocytes, and whose astrocyte-specific overexpression alleviates the symptoms of neurodegenerative diseases in mice.
In this study, Wang et al. show that the glycolytic metabolite phosphoenolpyruvate, produced by enolase 2, contributes to colorectal cancer malignancy and resistance to antiangiogenic therapy by inhibiting endogenous histone deacetylase 1 and favouring β-catenin signalling.
Dutta et al. show that impaired mitochondrial fatty acid synthesis (mtFAS) leads to neurodegeneration, increased ceramide levels and disturbed iron metabolism in flies and in fibroblasts from individuals with a mutation in an mtFAS enzyme.
Here Mukherjee et al. characterize the bidirectional communication between adipose tissue and ovarian cancer cells and show that adipocytes instruct cancer cells to divert glycolytic glycerol-3-phosphate towards lipid synthesis, thus promoting metastasis.
The authors identify a role for GABRA5 neurons in the lateral hypothalamus for energy balance regulation. Inhibiting these neurons increases weight gain and lipid accumulation through a process dependent on astrocytic GABA release.
Perszyk et al. identify the neural basis for odour-imagery ability and show that it indirectly predicts weight-gain susceptibility through a mechanism that is dependent on food-cue reactivity.
In this study, Okreglak et al. identify dynamic regulation of pH in the lysosome-like vacuole of growing S.cerevisiae cells and link pH dynamics in this subcellular compartment to amino acid release into the cytoplasm to meet metabolic demands during cell cycle progression.
Minogue et al. show that glutarate, a metabolite derived from tryptophan catabolism, has the ability to shape anti-tumour T cell responses by modulating pyruvate handling and alpha-ketoglutarate-dependent dioxygenases.