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Barreby et al. identify a distinct subpopulation of human resident liver myeloid cells that expresses factors that act in a protective fashion against oxidative stress associated with NAFLD.
Time-restricted feeding in the resting period is a potent dietary regimen to enhance running endurance in mice, by synchronizing rhythms of perilipin-5 in muscle tissues through involvement of the circadian clock.
Beals, Kayser et al. demonstrate that exercise, in conjunction with diet-induced weight loss, causes greater improvement in whole-body insulin sensitivity than matched diet-induced weight loss alone in people with obesity and prediabetes.
In aneuploid cancer cells with high ROS levels, a mitotic NADPH upsurge is required for error-free mitosis and tumour progression and therefore constitutes a cell cycle-dependent metabolic vulnerability.
Marine cyanobacteria contribute to global carbon balance by fixing CO2 and the shift between CO2 fixation and ATP production requires fine-tuning its metabolic fluxes to light–dark cycles. These cycles can be very short in marine environments due to sea currents and fast adaptation is key to avoid futile cycles. In this study, Lu et al. provide a mechanistic insight into how this process is tightly regulated.
Single-cell transcriptomic analysis of human multipotent progenitor cells reveals that upon adipogenic stimulation, Wnt signaling regulates the generation of functional multipotent mesenchymal progenitors, named structural Wnt-regulated adipose tissue resident cells, which maintain the progenitor pool.
In this study, Qian et al. identify a crosstalk between branched-chain amino acid metabolism and cell growth and motility through RhoC. Their work shows how enhanced BCAT1 activity, as identified by a mutation enriched in gastric cancer, leads to increased production of a metabolite that activates RhoC signaling.
Single-cell transcriptomic analysis of progenitor cells from human adipose depots reveals an adipogenic and a structural branch of cells, the latter named SWAT cells and shown to display a multipotent phenotype.
In this study, Park, Haley, Le, Jung et al. perform a detailed characterization in vivo of metabolic flux distribution during thermogenesis and uncover brown fat nutrient fluxes and unexpected inter-organ metabolic crosstalk and glutamine utilization.
Benedetti et al. produce a Cancer Atlas of Metabolic Profiles from 988 metabolomic and transcriptomic tissue profiles across 15 studies to analyse and identify gene–metabolite interactions that transcend cancer types.
Brain responses to food are severely diminished in individuals with obesity, and are not improved by 10% body weight loss. These findings point to an important role for the brain in weight regain after weight loss.
In this study, Weiss, Palmieri et al. show that macrophage-derived itaconate impinges on hepatocyte lipid metabolism. This mechanism participates in the crosstalk of the immune system with hepatocytes during the development of non-alcoholic fatty liver disease.
Glunk et al. explore target genes and cellular mechanisms related to a metabolic obesity with normal-weight phenotype, and identify a non-coding variant that affects actin remodelling in subcutaneous adipocytes, which in turn affects the capacity of these cells to accumulate lipids.
Using ultrasound to activate noninvasively specific neurons in the hypothalamus, a temporary hypothermic and hypometabolic state is induced in rodents.
Anatomically resolved maps of small molecules along the gut of colonized and germ-free mice reveal distinct spatial patterns throughout the gut. These patterns can, in part, be associated with specific microorganisms producing bioactive compounds.
Previous work using chemical inhibitors has reported the need for the mitochondrial pyruvate carrier for the classical activation of macrophages. In this study, Ran, Zhang et al. use a genetic approach to show that LPS-stimulated macrophage activation does not require the import of pyruvate into mitochondria.
Lin et al. show that small extracellular vesicles derived from SIRT2-deficient hepatocytes inhibit osteoclast differentiation from mouse and human bone-marrow-derived monocytes and alleviate bone loss in mouse models of osteoporosis.
Wang et al. show that the RNA methyltransferase Mettl3 contributes to hepatic sphingolipid homeostasis by promoting RNA decay of the sphingomyelinase Smpd3 during postnatal liver development, with Mettl3 deficiency leading to ceramide accumulation and liver developmental defects.