In a groundbreaking discovery that sheds new light on the metabolic underpinnings of atherosclerosis, researchers have illuminated the pivotal role of the amino acid glutamine in controlling macrophage behavior within arterial plaques. The study, led by Benhmammouch et al. and published in Nature Metabolism in 2025, elucidates how the critical membrane transporter SLC7A7 orchestrates glutamine uptake and subsequent glutaminolysis, thereby shaping macrophage restorative functions essential for plaque stability.

How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...

Chemotherapy reduces glucose transporter expression and glucose uptake in cancer cells, leading to decreased pyruvate levels. This decline prompts ACAT1-mediated acetylation of ME2 at Lys156, enhancing ME2 activity and promoting lactate production from glutamine. This ME2-dependent pathway is crucial for DNA repair protein lactylation and chemoresistance under conditions of low intracellular glucose. Abstract Lactate derived from aerobic glycolysis is crucial for DNA damage repair and chemoresistance. Nevertheless, it is frequently noted that cancer cells depend on glutaminolysis to replenish essential metabolites. Whether and how glutaminolysis might enhance lactate production and facilitate DNA repair in cancer cells remains unknown. Here, it is shown that malate enzyme 2 (ME2), which metabolizes glutamine-derived malate to pyruvate, contributes to lactate production and chemotherapy resistance in ovarian cancer. Mechanistically, chemotherapy reduces the expression of glucose transporters and impairs glucose uptake in cancer cells. The resultant decrease in intracellular glucose levels triggers the acetylation of ME2 at lysine 156 by ACAT1, which in turn potentiates ME2 enzyme activity and facilitates lactate production from glutamine. ME2-derived lactate contributes to the development of acquired chemoresistance in cancer cells subjected to prolonged chemotherapy, primarily by facilitating the lactylation of proteins involved in homologous recombination repair. Targeting ACAT1 to inhibit ME2 acetylation effectively reduced chemoresistance in both in vitro and in vivo models. These findings underscore the significance of acetylated ME2-mediated lactate production from glutamine in chemoresistance, particularly under conditions of reduced intracellular glucose within cancer cell, thereby complementing the Warburg effect and offering new perspectives on the metabolic links to chemotherapy resistance.

Glutamine metabolism is essential for T cell activation and functions. The inhibition of glutaminoly

Viruses are obligate intracellular parasites that rely on host cell metabolism for successful replic

Glutamine is best known to replenish the TCA cycle through glutaminolysis. Surprisingly, Zhu et al. discover that mitochondrial glutamine import (MGI) functions independently of glutaminolysis in cancer by sustaining Gln-mt-tRNAGln biosynthesis for mitochondrial translation, thus maintaining electron transport chain integrity. Targeting MGI represents a potential strategy to abrogate mitochondrial function in cancer.

SARS-CoV-2 infections in children lead to symptoms from mild respiratory illness to severe postacute sequelae of COVID-19, including multisystem inflammatory syndrome in Children (MIS-C). We conducted a metabolic profiling of 147 children’s serum samples, including acute COVID-19 patients, MIS-C patients, and healthy controls. Using nuclear magnetic resonance spectroscopy and liquid chromatography–mass spectrometry, we measured 1101 metabolites. The results revealed distinct metabolic profiles in acute COVID-19 and MIS-C patients, with significant alterations in lipid classes. Both conditions exhibited an elevated Apo-B100/Apo-A1 ratio and increased serum inflammatory markers. MIS-C patients showed unique disruptions, including increased triglycerides and altered lipoprotein composition. Despite milder clinical respiratory symptoms, children’s metabolic disturbances mirrored those seen in severe adult COVID-19 patients, indicating a shared inflammatory response to SARS-CoV-2. This suggests potential long-term health impacts, underscoring the need for continued research into the metabolic consequences of COVID-19 in children.

Recent evidence highlights the critical role of immune metabolism in the pathogenesis of rheumatoid arthritis (RA). We previously demonstrated that glutaminase 1 (GLS1), a key enzyme in glutamine meta...