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In this study, Kagan et al. highlight the relevance of adequate cardiolipin homeostasis by offering mechanistic insight into the pathogenesis of Barth syndrome. The study shows how altered accumulation of mono-lyso-cardiolipin, one of the derivatives of the mitochondrial lipid cardiolipin, forms an anomalous peroxidase complex with cytochrome c, thus leading to increased oxidation of polyunsaturated phospholipids.
Kovatcheva et al. show that vitamin B12 improves the efficiency of in vivo reprogramming and tissue repair through its functions in one-carbon metabolism and epigenetic modulation.
In this study, Rabah et al. investigate glucose usage in the brain, and show how glial cells transfer glycolysis-derived alanine to neurons in a fly model, thus supporting memory formation in cholinergic circuits.
PDK4-dependent lactate production by senescent stromal cells is shown to promote cancer growth and drug resistance and might have a broader role in the emergence of age-associated diseases.
In this study, Fu et al. provide mechanistic insight into how GLUT2 fine-tunes environmental nutrient sensing with T cell activation, which optimizes metabolic adaptation during acquisition of T cell effector function.
Gut-derived ammonia mediates stress responses in the host by maintaining brain glutamine availability, uncovering a gut–brain signalling basis for emotional behaviour.
Defects in interleukin-22 production and group 3 innate lymphoid cells are correlated with aggravated gut inflammation. Wu et al. find that proline uptake via the proline transporter Slc6a7 is involved in activation of lymphoid tissue inducer cells and interleukin-22 production in the gut, and that dietary supplementation with proline alleviates colitis in a mouse model.
Guhathakurta et al. describe the acetyltransferase activity of MOF in the mitochondria. MOF can acetylate COX17, thus contributing to the assembly and function of respiratory complex IV. These findings provide better understanding of how mitochondrial function is fine-tuned by acetylation.
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.
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.
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.