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Zhang et al. use human studies and mechanistic work in mouse models to describe how leucine serves as the key amino acid derived from dietary protein to drive deleterious macrophage mTORC1 signalling and promote cardiovascular disease.
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.
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.
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.
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.
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.
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.
Higher milk intake is associated with lower type 2 diabetes risk in lactase non-persistent individuals, partly through gut microbiome and blood metabolites.
During ageing, S-adenosylmethionine (SAM) is depleted from muscle stem cells (MuSCs) because of increased synthesis of the polyamine spermidine, leading to loss of heterochromatin and dysfunction of MuSCs. SAM restoration rescues the mouse MuSC defects.
Yu et al. show that inhibition of p21-activated kinase 4 (PAK4) ameliorates insulin resistance and enhances lipolysis by reducing phosphorylation of fatty acid-binding protein 4 (FABP4) and hormone-sensitive lipase (HSL). In parallel, PAK4 inhibition increases energy expenditure.
Stegen et al. show that serine metabolism is transiently upregulated during osteoclastogenesis, and it drives osteoclast differentiation via epigenetic regulation of NFATc1 expression.
Using several orthogonal loss-of-function approaches, Huang et al. provide a detailed assessment of the quantitative contribution of δ cell paracrine signalling to the glycaemic set point in mice.
Zhang et al. show that in mice, an adipocyte population with high expression of the transcription factor JunB in the brown adipose tissue shows reduced thermogenic capacity. Depletion of JunB increases the fraction of adipocytes with high thermogenic capacity and ameliorates diet-induced insulin resistance.
Todorova et al. characterize the strategies through which embryos secure amino acid supply during the early phases of development. Their findings show that, in the preimplantation phase, embryos uptake whole proteins through macropinocytosis and, over time, they shift towards soluble amino acid uptake. This strategy may contribute to protecting embryos from nutrient fluctuations.
Wei et al. show that proteolytic cleavage of fatty acid synthase (FASN) upon stress contributes to stress resolution. This role in stress resolution of the resulting C-terminal fragment of FASN is independent of its canonical function in fatty acid synthesis.
Iron is shown to have a central role in senescence, both by triggering senescence and through its accumulation in senescent cells, which is driving the senescence-associated secretory phenotype and, in turn, promotes fibrogenesis.
In this study, Papalazarou et al. screen the solute carrier family and identify candidates involved of serine transport in colorectal cancer cells. They further characterize cytosolic SLC6A14 and mitochondrial SLC25A15 as mediators of adequate serine supply to sustain cancer cell proliferation.
Shoop et al. develop mitoARCUS, a mitochondria-targeted nuclease with high specificity, to correct a relatively common pathogenic mtDNA mutation, allowing for beneficial shifts in heteroplasmy while reducing nuclear off-target gene editing.
Efferocytosis-induced macrophage proliferation is supported by increased non-canonical upregulation of glycolysis. Ngai, Schilperoort and Tabas provide mechanistic insight to understand how glycolysis-derived lactate contributes to this process by stabilizing MYC via extracellular signalling.