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Tighanimine et al. perform integrative time-resolved transcriptome and metabolome analysis in senescent cells and find that glycerol-3-phosphate and phosphoethanolamine accumulate and rewire lipid metabolism to promote senescence.

Continuous glucose monitoring (CGM) is increasingly being used to collect and evaluate data on glycaemic control for research purposes. However, the use of CGM in research settings requires proper understanding and handling of these devices for correct data collection and interpretation.

Selenium is usually incorporated into selenoproteins, with important functions in redox regulation. A new study in Nature Metabolism reveals a previously unappreciated role for selenium-based chemical species as direct electron donors to reduce ubiquinone, thus contributing to redox homeostasis by preventing lipid peroxidation.

Lee, Park et al. show that selenium has the ability to directly regulate the redox state of ubiquinone by donating electrons from hydrogen selenide via sulfide quinone oxidoreductase, thus preventing lipid peroxidation.

The prevailing notion that mitochondrial diseases arise from ATP deficiency is challenged by recent evidence that oxidative phosphorylation defects trigger maladaptive stress responses consuming excess energy. We argue that this chronic state of hypermetabolism imposes energetic constraints, thus causing mitochondrial disease pathophysiology, calling for careful translational studies from organelle to organism.

Ramachandran et al. identify a previously unappreciated function for transcriptional repressor B cell lymphoma 6 (BCL6) in muscle proteostasis and strength, and provide mechanistic insight into the molecular underpinnings of this function.

Veniant et al. report here on a GIPR antagonist conjugated to GLP-1 analogues that reduces body weight and improves metabolic markers in preclinical and phase 1 clinical settings.

High-fat diet (HFD) causes mitochondrial dysfunction in white adipocytes. A study in Nature Metabolism identifies the small GTPase RalA as a culprit in mice. Upon HFD, RalA activates the fission protein Drp1 to cause mitochondrial fragmentation and dysfunction, linking mitochondrial fuel utilization in white adipocytes to systemic lipid metabolism.

Xia et al. show that the activity of the small GTPase RalA is increased in white adipocytes in diet-induced obese mice. RalA enhances mitochondrial fission and therefore reduces energy expenditure, which contributes to weight gain.

Here, we reveal functional heterogeneity among β cells and discover that readily releasable β cells (RRβs) are a subpopulation that disproportionally contributes to biphasic glucose-stimulated insulin secretion. We further show that the dysfunction of RRβs has a crucial role in the progression of diabetes.

The field of personalized nutrition hypothesizes that ‘big data’ — biological, behavioural, social and environmental — can be leveraged to make more precise and effective dietary recommendations to individuals for improving health outcomes, compared to generic dietary advice. This article describes the research questions that need to be answered to understand whether personalized nutrition brings additional clinical utility.

This study reveals functional heterogeneity at the level of exocytosis among β cells and identifies a subpopulation of β cells that make a disproportionally large contribution to insulin release from mouse islets.

Kwak et al. identify a mixture of monogenic, rare and common genetic variants of youth-onset type 2 diabetes (T2D), highlighting the heterogeneity of youth-onset T2D and positioning it on a genetic spectrum between monogenic diabetes and adult-onset T2D.

This month, Nature Metabolism turns five. For a young journal such as ours, this anniversary represents a milestone worth celebrating, and a welcome opportunity to look back.

Demicco, Liu et al. discuss how metabolic adaptations in cancer contribute to tumour progression. These adaptations entail high spatial and temporal metabolic heterogeneity, based on local adaptations in different regions of the tumour microenvironment, as well as metabolic evolution over time as the tumour progresses and metastasizes.

Dwibedi et al. carry out a randomized controlled trial to evaluate whether subgroups of patients with diabetes could receive the greatest metabolic benefit from novel anti-diabetic drugs.

Miotto et al. show that in mice, liver-derived extracellular vesicles act on skeletal muscle and the pancreas and increase glucose effectiveness and insulin secretion, thereby modulating glycaemic control.

Genotype at the LCT locus determines lactase expression and very notably varies across populations. Milk intake variably influences the aetiology of the risk of type 2 diabetes depending on ancestry. In this issue of Nature Metabolism, Luo et al. describe how increased milk intake modifies both gut bacterial abundances and circulating metabolites in favour of decreasing the risk of type 2 diabetes in individuals who are lactase-deficient.

Higher milk intake is associated with lower type 2 diabetes risk in lactase non-persistent individuals, partly through gut microbiome and blood metabolites.