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Cancer cells have heightened demands for non-essential amino acids to support proliferation and redox homeostasis. Here, Zhang et al. propose the intersection of cysteine metabolism and polyamine synthesis as an unexplored metabolic vulnerability of cancer cells.
Transient glucose restriction after the activation of CD8+ TE cells ex vivo induces metabolic remodelling that enhances effector functions and tumour clearance in mice.
Levels of the glycolytic intermediate metabolite dihydroxyacetone phosphate are shown to signal cellular glucose availability to the mTORC1 complex through an AMPK-independent route.
Pluripotent stem cell–derived beta cells to treat type 1 diabetes are vulnerable to autoimmune destruction following transplantation. Using an in vivo CRISPR screen, Cai et al. identify RNLS as a modifier of beta cell vulnerability to autoimmune destruction.
Steinberg and colleagues show that long-chain fatty acyl-CoA esters are endogenous ligands for the drug-binding domain of AMPK β1–containing isoforms, and that such binding is critical for enhancement of fatty acid oxidation. These data may help explain how AMPK integrates responses to ketogenic diets, fasting or endurance exercise across distinct tissues in the absence of changes in adenine nucleotides.
Zhu and colleagues show that chronic activation of arcuate nucleus GABA+ neurons, agouti-related protein (AgRP) neurons alone or non-AgRP GABA+ neurons promotes severe obesity, but only inhibition of all GABA+ neurons can reverse the obese phenotype of hyperphagic mice, thus suggesting a redundant role for arcuate GABA+ neurons in obesity.
Chen et al. show that a prior history of hyperglycaemia can induce persistent DNA methylation changes at key CpGs to facilitate metabolic memory (the effect of early metabolic control on risk of developing diabetic complications later in life) and trigger diabetic complications, through modifying enhancer activity at myeloid and other cells.
Legouis et al. demonstrate that glucose synthesis from lactate in the renal proximal tubule is impaired during acute kidney injury (AKI), leading to metabolic abnormalities, which then contribute to increased morbidity and mortality of patients with AKI.
The muscular and organismal response to exercise training is reduced in animal models associated with chronic hyperglycaemia, thus suggesting that chronic hyperglycaemia inhibits aerobic adaptation to exercise.
Mi et al. report a super-enhancer signature in autosomal dominant polycystic kidney disease that regulates metabolic reprogramming during cystogenesis and controls cyst growth.
Brigger et al. show that adipose tissue eosinophil dysfunction with age underpins physiological features of ageing, including global inflammation, loss of physical fitness and myeloid skewing. Eosinophils transferred from young to aged mice reversed these features and improved immunological fitness in old age, in part via IL-4.
Zhu et al. show how cancer-associated fibroblasts (CAFs) regulate metabolism of branched-chain amino acids in pancreatic ductal adenocarcinomas. CAFs secrete and deliver branched-chain ketoacids to cancer cells by degrading proteins in the extracellular matrix that are internalized from the tumour microenvironment.
Cancer cells rely on selenium uptake and selenocysteine biosynthesis to avoid ferroptosis. However, this mechanism makes them dependent on SEPHS2, an enzyme in the selenocysteine biosynthesis pathway for the detoxification selenide that is produced during selenocysteine formation.
Maternal exercise, before and during pregnancy, has a beneficial effect on offspring. Harris et al. report that exercise-induced release of oligosaccharide 3′-sialyllactose in mouse breast milk mediates the metabolic health benefits of maternal exercise on offspring by improving glucose and insulin tolerance and cardiac function.
Modulating the capacity of the intestinal epithelium to catabolize fructose is shown to alter fructose-induced lipogenesis in the mouse liver, suggesting that fructose clearance in the small intestine protects from steatosis.
Lymphocytes encounter fluctuations in nutrient availability at sites of infection and inflammation. Wang et al. report that inosine can fulfil the metabolic needs of glucose-restricted anti-tumour effector CD8+ T cells.
Chronic obstructive pulmonary disease is a severe inflammatory lung disease characterized by obstructed airflow from the lungs. Here, Seimetz et al. show that NADPH oxidase subunit 1 (NOXO1) is responsible for peroxynitrite formation from nitric oxide and superoxide and drives the development of smoke-induced emphysema and pulmonary hypertension.
Here, Reilly et al. show that catecholamines control the balance between oxidation and re-esterification of fatty acids in white adipocytes through serine phosphorylation of STAT3, which inhibits the re-esterification enzyme GPAT3 via a non-genomic mechanism.
Hepatic bone morphogenetic protein 8b expression is shown to be induced in NASH to drive wound healing responses and NASH progression by promoting inflammatory pathways in hepatic stellate cells and, more broadly, in the liver parenchyma.
Proglucagon is expressed in various cell types and can be processed in distinct peptide hormone products. Here, Tellez et al. generate an immunocompromised mouse model that lacks only glucagon but maintains the production of the other peptides, and allows for measurement of glucagon secretion by human islets.