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Tumour necrosis factor is a classical pro-inflammatory cytokine. Sethi and Hotamisligil provide a comprehensive overview of its pleiotropic immunometabolic actions, while presenting a framework that is applicable to the complex network of other pro-inflammatory signals and their relevance to metabolic diseases such as obesity and diabetes.
By using an integrated omics approach, a landscape of metabolic remodelling of early-stage mouse embryogenesis is reconstructed, identifying key metabolites for epigenetic reprogramming.
While on a high-fat, high-calorie diet, a monthly cycle of 5 days of a fasting-mimicking diet can prevent obesity and related detrimental effects on cardiometabolic health and lifespan in mice.
Merlin et al. find that non-canonical glutamine transamination is required for macrophage efferocytosis in atherosclerotic plaques by sustaining redox buffering and fueling energy production for cytoskeletal rearrangements.
In this instalment of Career pathways, James White and Wenjing Du reflect on the importance of recruiting the right people, staying excited and making work and home life coexist.
Pharmacological inhibitors of fatty acid synthase, including the approved anti-obesity drug orlistat, are shown to inhibit replication of SARS-CoV-2 in vitro and in a mouse model of infection in vivo.
Over-nutrition is a major driver of obesity, but the mechanisms that promote and perpetuate it remain poorly understood. A recent study explores a role for umami taste in driving leptin resistance, hyperphagia and hypothalamic inflammation via overproduction of uric acid.
When is a calorie not just a calorie? In the current issue of Nature Metabolism, Roy et al. use recombinant inbred strains of mice to investigate the role of genetic background in the response to dietary fat. Notably, both lifespan and weight gain have been found to be highly dependent on genotype, thus highlighting the need for a personalized approach to dietary interventions.
Found in umami foods and known for their savoury taste, monosodium glutamate and inosine monophosphate are shown to induce metabolic syndrome in mice through induction of purine degradation in the liver and brain and through the formation of uric acid.
Patients with primary sclerosing cholangitis (PSC), a chronic cholestatic liver disease, display changes in the gut microbiota and in bile acid composition. Schneider, Candels and colleagues identify a role for microbiota-dependent regulation of bile acid synthesis through farnesoid X receptor signalling, which is relevant for PSC disease progression.
A combination of single-cell approaches, lineage tracing and metabolomics is used to characterize the changes to intestinal stem cell function in the small intestine that underlie intestinal maladaptation in mice fed an obesogenic diet.
Roy et al. quantify the impact of a high-fat diet across genetically diverse strains of mice, revealing a generally negative effect on lifespan but also a wide variability.
The maternal diet can impact offspring development, yet the mechanisms responsible for this remain largely unknown. New research shows that oocyte metabolites, specifically NAD+ and the methyl donor S-adenosylmethionine, can mediate the impact of maternal nutrient stress on the progeny through metabolic reprogramming in Drosophila.
When the ability of lymphatic vessels to transport fluid and macromolecules is perturbed, local adipose tissue often expands. Cao et al. identify destabilized, leaky mesenteric lymphatic vessels in obesity and demonstrate that correcting this dysfunction with a lymphatic-targeting drug improves systemic glucose metabolism.
Cao et al. find that the mesenteric lymphatic system becomes dysfunctional during obesity in mice and humans, leading to visceral adipose tissue accumulation and insulin resistance.
Hocaoglu et al. find a conserved shift in redox metabolites in fly oocytes and mammalian cells in response to mitochondrial respiratory quiescence that leads to reprogramming of progeny metabolism.
Bidault et al. find that interleukin-4 activates SREBP1 to promote de novo lipogenesis that consumes NADPH to drive alternative activation of macrophages through the accumulation of reactive oxygen species.
Clearance of dMiro from the outer mitochondrial membrane is a prerequisite for mitophagy of dysfunctional mitochondria. Li et al. find that oxidative stress stabilizes dMiro via its interaction with dMIC60. Dissociating this complex by genetic or pharmacologic interventions counteracts neurological aging in flies.