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Using holistic and reductionist approaches, Karunakaran et al. identify a causal association between higher expression of RIPK1 (a central regulator of inflammatory cell function) and the risk of obesity. RIPK1 induces activation of proinflammatory signalling in adipose tissue, promoting the accumulation of macrophages that drive metabolic inflammation and obesity simultaneously.
Linke et al. use unbiased and quantitative techniques to directly link both known and unknown liver and plasma lipid moieties to specific genomic loci, as compiled in a public web resource, LipidGenie. LipidGenie aided in the identification of a new group of sex-specific phosphatidylcholines.
After activation, conventional T cells undergo metabolic reprogramming. de Kivit et al. show that in human thymic regulatory T cells, TNFR2 stimulation promotes a glycolytic switch with a preferential glucose-derived carbon flux into the TCA cycle to support suppressive functions.
Electron transport chain (ETC) regulation can have important consequences for cellular bioenergetics. Here, Acín-Pérez et al. show that macrophage ETC regulation by the Fgr kinase can also affect systemic metabolism in the setting of diet-induced obesity.
Pharmacological targeting of de novo lipogenesis is an attractive clinical target for a wide range of diseases. Kelly et al. report that de novo lipogenesis is essential for platelet production in primates, but not in dogs and rats.
Xia et al. provide a method for deep learning of 3D facial images to predict biological age with an accuracy of ±2.8 yr from chronological age and its correlation with lifestyle indicators and blood transcriptomic age.
Carbohydrate metabolism in germ cells is shown to promote sugar appetite in female flies, thus demonstrating how metabolism in a subset of cells alters whole-animal behaviour.
Fructose consumption has greatly increased in recent years and has been linked to the development of hepatic steatosis. Here, the authors show that fructose promotes gut-barrier deterioration and subsequent endotoxaemia that in turn induces hepatic lipogenesis by activation TLR signalling in liver macrophages.
Whereas peripheral axons regenerate well after injury, axons located in the central nervous system, such as in the spinal cord, do not. Kong et al. identify AMPK as a regulator of neuronal regeneration and show that deletion of AMPKα1 promotes regeneration of injured spinal cord axons in mice.
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.
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.