Nature Metabolism, Published online: 23 September 2026; doi:10.1038/s42255-026-01645-2Author Correction: Uridine-sensitized screening identifies demethoxy-coenzyme Q and NUDT5 as regulators of nucleotide synthesis

Nature Metabolism, Published online: 23 September 2026; doi:10.1038/s42255-026-01631-8Rare diseases affect millions of people worldwide, yet they remain understudied. Six experts on rare metabolic diseases reflect on the state of the field and share their perspectives on the opportunities, challenges and emerging priorities for rare disease research.

Nature Metabolism, Published online: 22 September 2026; doi:10.1038/s42255-026-01637-2Author Correction: N6-methyladenosine (m6A) in 18S rRNA promotes fatty acid metabolism and oncogenic transformation

Nature Metabolism, Published online: 29 September 2026; doi:10.1038/s42255-026-01629-2MRMhub: a scalable data-processing framework for large-scale targeted metabolomics

Nature Metabolism, Published online: 29 September 2026; doi:10.1038/s42255-026-01615-8This study reports that chronic exposure to microplastic and nanoplastic particles differentially affects Kupffer cells, which impairs their function and has consequences on both liver and systemic metabolism.

Nature Metabolism, Published online: 21 September 2026; doi:10.1038/s42255-026-01614-9In the prospective, multicentre TEDDY study, distinct patterns of gut microbiome maturation are associated with differential risk of type 1 diabetes, with host genetics modifying the strength of this association.

Nature Metabolism, Published online: 25 September 2026; doi:10.1038/s42255-026-01641-6Short-chain fatty acids and blood pressure

Nature Metabolism, Published online: 18 September 2026; doi:10.1038/s42255-026-01594-wThe epitranscriptomic mRNA modification N6-methyladenosine (m6A) helps to maintain the functional identity of pancreatic α-cells. Deletion of the m6A writer METTL14 impairs amino acid-stimulated glucagon secretion, destabilizes the α-cell state and promotes plasticity towards immature, insulin-secreting β-cell-like fates.

Nature Metabolism, Published online: 18 September 2026; doi:10.1038/s42255-026-01591-zm6A methylation acts as an epitranscriptomic regulator of endocrine cell identity in pancreatic islet alpha cells, with loss of m6A leading to impaired alpha cell identity, α- to β-cell conversion and metabolic rewiring of islet endocrine cells.

Nature Metabolism, Published online: 17 September 2026; doi:10.1038/s42255-026-01613-wIn a 12-week pilot study, 20 people with early-stage Huntington’s disease restricted their eating to a daily 6–8-h window. The intervention was feasible and well-tolerated, and exploratory analyses suggested improvements in clinical measures, levels of plasma neurofilament light (a biomarker of neurodegeneration) and cellular bioenergetics.

Nature Metabolism, Published online: 17 September 2026; doi:10.1038/s42255-026-01612-xA 12-week pilot study suggests that time-restricted eating is well tolerated and associated with favourable clinical outcomes in individuals with early-stage Huntington’s disease.

Nature Metabolism, Published online: 23 September 2026; doi:10.1038/s42255-026-01645-2Author Correction: Uridine-sensitized screening identifies demethoxy-coenzyme Q and NUDT5 as regulators of nucleotide synthesis

Nature Metabolism, Published online: 23 September 2026; doi:10.1038/s42255-026-01631-8Rare diseases affect millions of people worldwide, yet they remain understudied. Six experts on rare metabolic diseases reflect on the state of the field and share their perspectives on the opportunities, challenges and emerging priorities for rare disease research.

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01633-6Author Correction: Asparagine deprivation enhances T cell antitumour response in patients via ROS-mediated metabolic and signal adaptations

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01603-yCombination therapy with retatrutide and cagrilintide lowers body weight and improves markers of metabolic health in obese, male rats more efficiently than equimolar monotherapies and matched-dose combinations incorporating semaglutide or tirzepatide.

Nature Metabolism, Published online: 22 September 2026; doi:10.1038/s42255-026-01637-2Author Correction: N6-methyladenosine (m6A) in 18S rRNA promotes fatty acid metabolism and oncogenic transformation

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01616-7Using a genome-wide CRISPR screen, the authors demonstrate that excess cysteine drives mitochondrial iron accumulation and iron–sulfur cluster failure, triggering a distinct iron-dependent cell death pathway.

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01620-xCells depend on cysteine, but excess free cysteine comes at a price. Nakamura et al. show that excess cysteine disrupts mitochondrial iron homeostasis, which drives a distinct iron-dependent cell death, revealing why cells rapidly channel cysteine into glutathione synthesis.

Nature Metabolism, Published online: 21 September 2026; doi:10.1038/s42255-026-01614-9In the prospective, multicentre TEDDY study, distinct patterns of gut microbiome maturation are associated with differential risk of type 1 diabetes, with host genetics modifying the strength of this association.

cGAS–STING signalling in intestinal epithelial cells modulates gut microbiome-derived indole-3-acetic acid production to regulate adipose thermogenesis and systemic metabolic health.

Rewiring of branched-chain amino acid catabolism in prostate cancer fuels propionyl-CoA synthesis, lysine propionylation and stabilization of SREBP2, leading to increased cholesterol and androgen synthesis, and thus promotes metabolic adaptation of cancer cells and disease progression.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01593-xArgininosuccinate synthase 1 (ASS1) phosphorylation is elevated in samples from patients with B cell acute lymphoblastic leukaemia and in leukaemic cells. As ASS1-derived argininosuccinate was found to activate cytosolic NT5C2 to promote purine nucleoside biosynthesis and replenish cellular carbon sources, ASS1 and NT5C2 are potential therapeutic targets for tyrosine kinase-driven haematological malignancies.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01588-8Early signs of cardiovascular–kidney–metabolic disease (CKMD) emerge before 20 years of age, but methods to identify CKMD risk in children are limited. We identified a proteomic and phenotypic signature of CKMD in children that is strongly associated with the development and clinical outcomes of CKMD in adulthood.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01623-8Great science comes in all shapes and sizes. Choosing the most suitable article type is key to managing the expectations of readers, editors and reviewers alike.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01589-7By linking cardiovascular–kidney–metabolic disease (CKMD) phenotypes to the proteome of children and adolescents, the authors show that paediatric CKMD proteomic signatures predict cardiometabolic disease outcomes in adulthood.

Nature Metabolism, Published online: 18 September 2026; doi:10.1038/s42255-026-01594-wThe epitranscriptomic mRNA modification N6-methyladenosine (m6A) helps to maintain the functional identity of pancreatic α-cells. Deletion of the m6A writer METTL14 impairs amino acid-stimulated glucagon secretion, destabilizes the α-cell state and promotes plasticity towards immature, insulin-secreting β-cell-like fates.

Nature Metabolism, Published online: 18 September 2026; doi:10.1038/s42255-026-01591-zm6A methylation acts as an epitranscriptomic regulator of endocrine cell identity in pancreatic islet alpha cells, with loss of m6A leading to impaired alpha cell identity, α- to β-cell conversion and metabolic rewiring of islet endocrine cells.

Nature Metabolism, Published online: 17 September 2026; doi:10.1038/s42255-026-01613-wIn a 12-week pilot study, 20 people with early-stage Huntington’s disease restricted their eating to a daily 6–8-h window. The intervention was feasible and well-tolerated, and exploratory analyses suggested improvements in clinical measures, levels of plasma neurofilament light (a biomarker of neurodegeneration) and cellular bioenergetics.

Nature Metabolism, Published online: 17 September 2026; doi:10.1038/s42255-026-01612-xA 12-week pilot study suggests that time-restricted eating is well tolerated and associated with favourable clinical outcomes in individuals with early-stage Huntington’s disease.

Nature Metabolism, Published online: 10 September 2026; doi:10.1038/s42255-026-01592-yAdipose tissue ALKBH5 responds to cold and adrenergic stimulation and improves stability of CKB mRNA by m6A demethylation, leading to increased energy expenditure and thermogenesis independent of UCP1 in mice.

Nature Metabolism, Published online: 09 September 2026; doi:10.1038/s42255-026-01624-7Author Correction: Lac-Phe induces hypophagia by inhibiting AgRP neurons in mice

Nature Metabolism, Published online: 09 September 2026; doi:10.1038/s42255-026-01611-yGVC-Calc enables large-scale analysis of continuous glucose monitoring data

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01633-6Author Correction: Asparagine deprivation enhances T cell antitumour response in patients via ROS-mediated metabolic and signal adaptations

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01634-5Author Correction: A glucose-like metabolite deficient in diabetes inhibits cellular entry of SARS-CoV-2

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01603-yCombination therapy with retatrutide and cagrilintide lowers body weight and improves markers of metabolic health in obese, male rats more efficiently than equimolar monotherapies and matched-dose combinations incorporating semaglutide or tirzepatide.

DHHC17-mediated palmitoylation promotes laminin-511 stabilization and availability in the liver metastatic niche, which decreases the cancer cell-killing capacity of neutrophils.

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01620-xCells depend on cysteine, but excess free cysteine comes at a price. Nakamura et al. show that excess cysteine disrupts mitochondrial iron homeostasis, which drives a distinct iron-dependent cell death, revealing why cells rapidly channel cysteine into glutathione synthesis.

Nature Metabolism, Published online: 15 September 2026; doi:10.1038/s42255-026-01616-7Using a genome-wide CRISPR screen, the authors demonstrate that excess cysteine drives mitochondrial iron accumulation and iron–sulfur cluster failure, triggering a distinct iron-dependent cell death pathway.

Nature Metabolism, Published online: 08 September 2026; doi:10.1038/s42255-026-01580-2In this issue of Nature Metabolism, Wu et al. reveal that cytosolic NADPH, a pentose phosphate pathway metabolite, drives a physiological cardiac hypertrophic response that is protective against heart attack injury and can be raised by a candidate spermidine derivative.

Nature Metabolism, Published online: 08 September 2026; doi:10.1038/s42255-026-01587-9NADPH derived from the pentose phosphate pathway is shown to mediate exercise-induced physiological cardiac hypertrophy and protect against damage caused by ischaemia–reperfusion injury.

Nature Metabolism, Published online: 07 September 2026; doi:10.1038/s42255-026-01586-wArgininosuccinate produced by phosphorylated ASS1 allosterically enhances the nucleosidase activity of NT5C2, resulting in increased production of purine nucleosides, which serve as a carbon source in BCR–Abl-positive haematological cancers.

The study reports a non-classical tocopherol pathway in Rhodobacter that enables heterologous α-tocopherol synthesis by bypassing DMPBQ via a γ/β-tocopherol methyltransferase.

Nature Metabolism, Published online: 04 September 2026; doi:10.1038/s42255-026-01622-9Author Correction: Impaired cAMP–PKA–CREB1 signalling drives mitochondrial dysfunction in skeletal muscle during cancer cachexia

Tang et al. reveal that macrophage-derived itaconate acts as a paracrine inhibitor of adipose tissue thermogenesis by blocking succinate uptake into brown adipose tissue.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01593-xArgininosuccinate synthase 1 (ASS1) phosphorylation is elevated in samples from patients with B cell acute lymphoblastic leukaemia and in leukaemic cells. As ASS1-derived argininosuccinate was found to activate cytosolic NT5C2 to promote purine nucleoside biosynthesis and replenish cellular carbon sources, ASS1 and NT5C2 are potential therapeutic targets for tyrosine kinase-driven haematological malignancies.

Nature Metabolism, Published online: 04 September 2026; doi:10.1038/s42255-026-01602-zAuthor Correction: Combined alcohol and cannabinoid exposure leads to synergistic toxicity by affecting cerebellar Purkinje cells

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01588-8Early signs of cardiovascular–kidney–metabolic disease (CKMD) emerge before 20 years of age, but methods to identify CKMD risk in children are limited. We identified a proteomic and phenotypic signature of CKMD in children that is strongly associated with the development and clinical outcomes of CKMD in adulthood.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01623-8Great science comes in all shapes and sizes. Choosing the most suitable article type is key to managing the expectations of readers, editors and reviewers alike.

Nature Metabolism, Published online: 11 September 2026; doi:10.1038/s42255-026-01589-7By linking cardiovascular–kidney–metabolic disease (CKMD) phenotypes to the proteome of children and adolescents, the authors show that paediatric CKMD proteomic signatures predict cardiometabolic disease outcomes in adulthood.

Nature Metabolism, Published online: 04 September 2026; doi:10.1038/s42255-026-01604-xMitochondrial homeostasis is tightly regulated to prevent hepatocyte injury. In this issue of Nature Metabolism, Wang et al. identify UBE2N as a switch that determines whether hepatocytes undergo protective mitophagy or pathogenic cell death in metabolic dysfunction-associated steatohepatitis (MASH).