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Dietary restriction promotes the expansion of effector T cells via ketone bodies, which enhances anti-tumour immunity and synergizes with immunotherapy in mice.
The microbial metabolite trimethylamine (TMA), the precursor of TMAO, which is associated with adverse cardiometabolic outcomes, is shown to have beneficial metabolic and anti-inflammatory effects in the host in the context of obesity.
A machine-learning-based computational approach to probe pathway coessentiality reveals that complex II of the electron transport chain regulates de novo purine synthesis, and can be targeted to treat acute myeloid leukaemia.
Age-related decline of chaperone-mediated autophagy blunts the regenerative capacity of muscle stem cells, partly due to impaired glycolytic shift required for normal stem cell expansion.
Chaperone-mediated autophagy declines with age in skeletal muscle of humans and mice, leading to muscle dysfunction characterized by impaired calcium homoeostasis and mitochondrial function.
In a mouse model of the rare disease citrin deficiency, the authors discovered that the accumulation of glycerol-3-phosphate leads to ChREBP activation and FGF21 induction. The study identifies glycerol-3-phosphate as a ChREBP-activating ligand, which could resolve paradoxes of FGF21 expression and clarify the logic of lipogenic transcription.
Tumour-induced dysregulation of cAMP–PKA–CREB1 signalling in skeletal muscle is shown to be a driver of mitochondrial dysfunction, contributing to cancer cachexia in mice.
Through an epigenome-wide blood analysis in children of mothers with or without type 1 diabetes, the authors identify epigenetic modifications of type 1 diabetes susceptibility loci through which maternal type 1 diabetes may protect from islet autoimmunity in offspring.
Barnett et al. disentangle the differential contribution of mitochondrial complex I- and complex III-derived ROS to astrocytic function, with CIII-derived ROS being a major driver of neuroinflammatory responses.
Inhibition of AMPK activation under low glucose conditions in oligodendrocyte precursor cells is shown to be important for myelination during development and remyelination in neuronal disorders.
The gut microbiota-derived metabolite indole-3-propionic acid (IPA) is found to enhance mitochondrial fatty acid and amino acid oxidation in CD4+ T cells. In mice, IPA-mediated metabolic reprogramming of CD4+ T cells exerts anti-inflammatory effects and protects against colitis.
Acetate accumulation and metastasis of hepatocarcinoma cells is driven by a metabolic interaction involving HCC-derived lactate and acetate secretion from tumour-associated macrophages.
Greda et al. show that sortilin and apolipoprotein E3 mediate import and utilization of long-chain fatty acids as a metabolic fuel in neurons after glucose restriction.
In the context of parental or diet-induced obesity, preweaning ketosis contributes to improved health outcomes, particularly by regulating the histone acetylome and β-hydroxybutyrylome for transcriptional activation of beige fat biogenesis genes.
The SWEET project is a multicenter, randomized, controlled trial that shows that long-term consumption of sweeteners and sweetness enhancers improves body weight control and elicits beneficial gut microbiota changes in adults with overweight or obesity.
Saber et al. show that the lipase DDHD2 provides endogenous saturated fatty acids to support fatty acid oxidation and energy production, proteostasis and membrane trafficking balance.
Persistent microglial activation upon ischaemic injury leads to the formation of stroke-associated foamy microglia, perpetuating long-term inflammation, white matter damage and functional impairments. These effects can be ameliorated by reducing microglial cholesterol overload through activation of CYP46A1.
