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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.
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.
Aregger et al. provide an approach to study genetic interactions in mammalian cells and describe genetic interaction maps that characterize genes involved in lipid metabolism. They identify the role of C12orf49, a previously uncharacterized gene, in regulating lipid uptake in human cells.
Thermogenic adipose tissue has been suggested as a potential target to treat metabolic diseases. Here, Tran et al. show that a long noncoding RNA, LINC00473, is induced during activation of thermogenic adipocytes and regulates energy metabolism through interorganelle communication.
Currently, there is no approved treatment for NAFLD and NASH. Here, Boland et al. show that the GLP-1R and GCGR dual-agonist cotadutide reduces hepatic steatosis, inflammation and fibrosis via GCGR agonism, and glucose homeostasis and weight gain by activating GLP-1 signalling.
Morphological changes in kidney glomerular ultrastructure and altered compression of the glomerular basement membrane are shown to correlate with albuminuria.
β-cell dysfunction in diabetes is caused by glucose and inflammation toxicity. Here, Fu et al. show that β-cell glucose metabolism can be protective though pyruvate carboxylase–mediated shunting of arginine to ureagenesis and away from toxic nitric oxide production, thus suppressing inflammation.
Wei et al. show that the chromatin regulator MRG15 interacts with the nuclear receptor LRH-1 and is rhythmically recruited to lipid- and cholesterol-biosynthetic genes. In a nutrient-rich state, MRG15 alters histone acetylation status to activate gene transcription and lipid synthesis, whereas in a nutrient-scarce state, MRG15 genomic recruitment and lipid synthesis are reduced.
Metabolic compensation equips tumours with the plasticity to circumvent individual nutrient pathway perturbation. Méndez-Lucas et al. demonstrate the power of synergistic targeting of multiple metabolic pathways to stymie liver tumourigenesis.
Yang et al. report that adenosine kinase possesses NRH kinase activity that enables it to convert NRH into NAD+, thus revealing a new salvage pathway for NAD+ biosynthesis operating in mammalian cells.
Tumour recurrence is a common cause of death for patients with cancer. Here Fox et al. show how the antioxidant transcription factor Nrf2 is activated in dormant residual tumour cells and promotes their proliferation and tumour growth by inducing a metabolic reprogramming aimed to maintain redox homeostasis and nucleotide synthesis.
The ventromedial nucleus of the hypothalamus is known to maintain energy homeostasis by controlling locomotor activity and thermogenesis. Here van Veen and Kammel et al. identified heterogeneous neuronal populations with sexually dimorphic gene expression and functions by using single-cell RNA analysis.