Nature Metabolism自然·代谢
Nature Metabolism(英文缩写 NAT METAB),ISSN 2522-5812,eISSN 2522-5812,中文译名:自然·代谢 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
Nature Metabolism 最新收录文献
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2. Rare science, real impact: shaping the future of research on rare metabolic diseases.
PMID:日期:2026-09-23该文献暂无摘要。
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4. Gut microbiome maturation in early childhood interacts with host genetics to predict type 1 diabetes risk.
PMID:日期:2026-09-21Prospective evidence linking early-life microbiome development and host genetics with type 1 diabetes (T1D) risk is limited. Here, we describe how gut microbiome maturation and host genetics influence T1D risk in the TEDDY study. We analysed 12,151 longitudinal metagenomes and host genetic data from 887 children at high genetic risk for T1D followed for up to 6 years. We identify three microbiome maturational patterns: Early Matured, Late Matured and Early Plateaued, driven primarily by non-linear changes in species from the Bifidobacterium and Ruminococcus genera. The Early Matured pattern is enriched in galactose metabolism and exhibits higher production of aromatic amino acids and B-group vitamins at early follow-ups, whereas the Early Plateaued pattern has increased microbial production of branched-chain amino acids. Notably, the Early Plateaued pattern is associated with a threefold elevated risk of T1D, whereas other patterns are not associated with T1D risk. Furthermore, we find that host genetic variants related to antimicrobial and antiviral immune responses modify the association between the Late Matured pattern and T1D risk. These findings highlight the role of early microbial exposures and host genetics in T1D susceptibility.
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5. Meal timing as medicine: clinical evidence for intermittent fasting in Huntington's disease.
PMID:日期:2026-09-17该文献暂无摘要。
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6. Effects of time-restricted eating in early-stage Huntington's disease: a pilot study.
PMID:日期:2026-09-17Time-restricted eating (TRE) has shown neuroprotective potential in preclinical models of Huntington's disease (HD) but has not been tested clinically. Here, we report the results of a 12-week open-label pilot trial ( NCT06490367 ) of 8-h TRE, alongside standard-of-care diet and activity recommendations, in 20 individuals with early-stage HD. We show that TRE is feasible, well tolerated and associated with favourable changes in clinical measures of HD and plasma neurofilament light levels. Overall, these results support the need for further investigation of TRE as a potential lifestyle intervention in HD.
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7. Author Correction: A glucose-like metabolite deficient in diabetes inhibits cellular entry of SARS-CoV-2.
PMID:日期:2026-09-15该文献暂无摘要。
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10. Cysteine excess triggers a mitochondrial iron-dependent cell death.
PMID:日期:2026-09-15Thiol-containing metabolites are central to cellular redox homeostasis. Among these, cysteine functions as a proteogenic amino acid, supports redox balance and iron-sulfur cluster biogenesis, and, when depleted, triggers ferroptosis. Cells nevertheless maintain cysteine at low levels, reflecting its intrinsic toxicity, but the mechanisms by which excess cysteine causes cell death remain unclear. Here we performed a genome-wide CRISPR screen and identified mitochondrial iron transporters as essential mediators of cysteine toxicity. Limiting mitochondrial iron availability suppresses cysteine-induced cell death and prevents impairment of iron-sulfur cluster proteins and respiration. Mechanistically, cysteine mobilizes iron from ferritin, expands the cytosolic iron pool and drives mitochondrial iron accumulation. Enhancing glutathione reductase activity specifically within mitochondria restores redox balance downstream of iron accumulation and protects cells by maintaining iron-sulfur cluster integrity. Our findings suggest that maintaining low cysteine levels safeguards mitochondrial iron homeostasis, and that excess cysteine triggers a distinct mitochondrial iron-dependent cell death under conditions of thiol imbalance.