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Doke et al. show that NMN and NR supplementation has protective effects on kidney injury by preventing cisplatin-induced release of cytosolic mitochondrial RNA and subsequent activation of the RIG-I pathway and inflammation.
The metabolomics literature suffers from ambiguity in the nomenclature for individual metabolites, which introduces a disconnect between publications and leads to misinterpretations. This Comment proposes recommendations for metabolite annotations to engage the scientific community and publishers to adopt a more consistent approach to metabolite nomenclature.
Sympathetic innervation of brown and white adipose tissue is shown to be promoted by zinc released from thermogenic adipocytes, revealing a positive feedback mechanism for regulation of thermogenesis and thereby energy expenditure.
Primary cilia are shown to adjust length in response to cellular nutrient availability, with a special role for glutamine-mediated anaplerosis via the enzyme ASNS, which was found to be located at the base of cilia. Consistently, cells lacking cilia show an altered response to glutamine during metabolic stress.
Both cell cycle arrest and secretions of senescent cells are subject to metabolic control. In this issue of Nature Metabolism, Roh et al. show that lysosomal partitioning of cholesterol potentiates inflammatory secretion during senescence.
Senescenct cells are shown to accumulate cholesterol in lysosomes, which upregulates mTORC1 signaling, thereby supporting the senescence-associated secretory phenotype and promoting senescence-associated inflammation.
Scientific meetings are the perfect venue for staying on top of the field and building new relationships with researchers from all career stages, as well as solidifying bonds with current authors. Here we explain why editors of Nature Metabolism attend conferences and what we do when we get there.
Takhaveev et al. use single-cell methods and mathematical modeling to reveal distinct waves in the synthesis rates of proteins, lipids and polysaccharides during the budding yeast cell cycle and relate them to flux changes in primary metabolism.
By measuring protein abundance in blood using high-throughput antibody-based techniques, a genetic map of blood proteins in humans replicates findings from much larger studies, uncovers hundreds of new signals and bridges genetic variation to multiple diseases.
Identifying mechanistic pathways that link obesity with COVID-19 severity provides targets for interventions to reduce the high risk of severe outcomes owing to obesity. The authors of a recent study use genomics and proteomics to show that nephronectin could be involved in one of these pathways.
How obesity contributes to COVID-19 severity is not fully understood. In this study, Yoshiji et al. found that the plasma protein nephronectin partially mediates the effect of obesity on the risk of COVID-19 severity using a two-step Mendelian randomization approach and omics analyses.
The rate of glycolysis increases markedly during the phagocytosis of apoptotic cells and upon macrophage activation by inflammatory stimuli. However, the motive for burning glucose differs in both conditions.
Schilperoort et al. explore the mechanisms underlying dynamic changes in macrophage metabolism that support efferocytosis. They show that transient glycolysis and subsequent lactate production are necessary to execute continual efferocytosis, as opposed to prolonged glycolysis observed in pro-inflammatory macrophages.
The authors provide evidence in mice and humans showing that parenteral nutrition impairs glucose and insulin homeostasis by altering the gut microbiota and its metabolites.
The alternative splicing landscape of pancreatic islets is dominated by an evolutionarily conserved program of microexons. These short exons encode only a few extra amino acids in genes related to hormone secretion. Microexons are important to islet function, affecting glycaemic control and the risk of type 2 diabetes.
In this study, Juan-Mateu et al. discover microexons that modulate insulin secretion in the pancreas in response to glucose levels in beta cell lines and mouse islets. Human genetic variants modulating these islet microexons are associated with type 2 diabetes risk.