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Long-acting GIPR agonists, individually or as part of GIPR–GLP-1R co-agonists, are shown to require GIPR signaling in inhibitory GABAergic neurons to decrease body weight and food intake in mice.
In this study, Kreuzaler et al. perform zonal analysis to study metabolic heterogeneity in breast cancer and identify the metabolic dependency on pantothenic acid (vitamin B5) in areas of the tumor that show high expression levels of the oncogene MYC. Dietary restriction of vitamin B5 reverses several MYC-driven metabolic changes and hampers tumor progression.
Neuronal energization and memory formation in the fruit fly are found to be conditioned by the shuttling of alanine between glial cells and neurons. This observation highlights the emerging role of energy metabolism as a driver of tissue function.
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.
Nature Metabolism is launching a joint collection of articles focusing on dietary interventions to improve cardiometabolic health, together with Nature Communications, npj Metabolic Health and Disease and Scientific Reports.
Glucose transporter-mediated uptake of glucose is a key metabolic checkpoint in T cells. Fu et al. have identified GLUT2 as a critical regulator of CD8+ T cell metabolism and function in response to glucose and oxygen availability.
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.
This Review article discusses how the emerging field of metabolomic epidemiology gives insight into the aetiology of various diseases and how these findings could be translated into clinical applications.
Gut-derived ammonia mediates stress responses in the host by maintaining brain glutamine availability, uncovering a gut–brain signalling basis for emotional behaviour.
Analysis of cells shed from the mouse gut, using bulk and single-cell transcriptomics, as well as single-molecule FISH and intravital imaging, revealed that shed cells are diverse, remain viable for a few hours and upregulate anti-microbial gene expression programs.
Group 3 innate lymphoid cells (ILC3s) maintain intestinal barrier integrity and nutrient absorption via IL-22; however, little is known about how these immune cells fuel effector function. Wu et al. now report that uptake of dietary proline acts as a critical metabolic modulator of the ILC3 transcriptome and cytokine production to maintain gut health.
Bahar Halpern et al. use bulk and single-cell RNA sequencing of intestinal faecal washes to show that intestinal epithelial cells remain viable after being shed. Alongside shed immune cells, these epithelial cells may contribute to immune regulation in the intestine.
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.
Mitochondrial proteins are frequently acetylated, but most of these modifications are thought to occur non-enzymatically, rather than requiring an acetyltransferase. A new study by Akhtar and colleagues challenges this view by demonstrating that MOF, a well-characterized histone acetyltransferase, bolsters mitochondrial metabolism by acetylating the complex IV assembly factor COX17.
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.
Bilal Sheikh and Yuxiong Feng share their scientific journey and how it has taken them around the world and given them freedom to pursue their curiosity and own ideas. They share the passion that drives their research and highlight the importance of building a strong, collaborative and complementary team.