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Gates et al. show that histone butyrylation and propionylation in the intestinal epithelium are regulated by the gut microbiota and histone butyrylation is associated with gene regulatory programmes.
The authors show that abnormal elevation of osteocyte-derived sclerostin deregulates Wnt–β-catenin signalling in the brain and aggravates cognitive impairment under pathological conditions.
In a randomized placebo-controlled trial in 37 individuals with excess body weight, dietary supplementation with resistant starch lowers body weight and induces changes in gut microbiota composition. Mechanistic analysis in male mice shows that resistant starch at least partially facilitates weight loss through the action of Bifidobacteriumadolescentis.
In the context of succinate uptake to promote adipose tissue browning, Reddy, Winther et al. show how the directionality of succinate transport across membranes is coupled with metabolic flux-derived changes in pH gradients.
De Solis and Del Río-Martín et al. investigate the reciprocal interplay between AgRP and POMC neurocircuits that governs the precise regulation of food intake and systemic metabolic homeostasis.
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.
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.
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.
Electron-transfer flavoprotein dehydrogenase (ETFDH) is shown to associate with mitochondrial complex III (CIII) physically and functionally, thereby promoting electron channelling to increase CIII efficiency.
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.