Cell Metabolism

Cell metabolism encompasses the integrated network of biochemical reactions by which cells harvest and allocate energy, build macromolecules and maintain redox and ionic balance. Catabolic pathways break down nutrients—carbohydrates, lipids and amino acids—into smaller units, generating ATP and reducing equivalents (NADH, NADPH) that power cellular work. Anabolic pathways use that energy to assemble complex polymers such as proteins, nucleic acids and membrane lipids. Mitochondria serve as the principal hub for oxidative phosphorylation, converting the products of glycolysis and the tricarboxylic acid cycle into ATP through electron‐transport-coupled proton translocation. Metabolic flux is finely tuned at multiple levels: substrate availability, allosteric regulation of key enzymes, covalent modification and the dynamic formation of enzyme assemblies. Central nutrient and energy sensors—AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR) and the cellular redox state—coordinate anabolic and catabolic demands with environmental cues. Dysregulation of these networks underlies obesity, diabetes, cardiovascular disease and cancer, while adaptive remodelling of metabolism supports cell differentiation, stress tolerance and immune function. Advances in lipidomics, flux analysis and organelle-specific metabolomics have revealed new metabolic checkpoints and inter-organ communication routes that shape systemic homeostasis and offer novel therapeutic targets.

Research from Nature Portfolio

Sympathetic neuron–derived neuropeptide Y was shown to sustain the perivascular niche of adipocyte progenitors in both white and brown fat depots. By maintaining proliferative thermogenic precursors, this mechanism preserves energy expenditure and protects against diet-induced weight gain without altering food intake or core metabolic set-points.

Transient, post-prandial surges of interleukin-1β directly target early-stage adipocyte precursors, rapidly up-regulating C/EBPβ and C/EBPδ to enhance white adipogenesis. In contrast, chronic IL-1β elevation impairs this homeostatic remodelling, highlighting the dual role of an inflammatory cytokine in nutrient buffering and tissue expansion.

A novel assembly state of mitochondrial Complex II, termed CIIlow, was identified as a bioenergetic checkpoint under energy stress. CIIlow accumulation restrains de novo pyrimidine synthesis and enforces S-phase arrest. Loss of CIIlow leads to unchecked nucleotide production and cell-cycle progression, a vulnerability that is exploited in SDH-mutant tumours where restoration of CIIlow rescues metabolic homeostasis.

Cell Metabolism publication trend

The graph below shows the total number of articles in cell metabolism across all publications each year (not limited to Nature Index journals).

Technical terms

Catabolism: Metabolic pathways that break down complex molecules to release energy and reducing equivalents.

Anabolism: Biosynthetic pathways that construct macromolecules from simpler precursors using ATP and NADPH.

Oxidative phosphorylation: Mitochondrial process by which electrons flow through respiratory complexes to drive ATP synthesis via a proton gradient.

Redox state: The balance of oxidised and reduced electron carriers (e.g., NAD+/NADH, NADP+/NADPH) that governs cellular oxidative reactions.

Thermogenic adipocyte: A fat cell subtype containing abundant mitochondria and uncoupling proteins, specialised for heat production via proton leak.

Adipogenesis: Differentiation of mesenchymal progenitors into mature lipid-storing adipocytes.

Enzyme allostery: Regulation of enzyme activity by binding of effectors at sites distinct from the active site, altering catalytic efficiency.

Metabolic flux: The flow rate of metabolites through a metabolic pathway, reflecting the integrated control of enzyme activity, substrate supply and energy demand.

References

1. Sympathetic neuropeptide Y protects from obesity by sustaining thermogenic fat. Nature (2024).
2. IL-1β promotes adipogenesis by directly targeting adipocyte precursors. Nature Communications (2024).
3. Alternative assembly of respiratory complex II connects energy stress to metabolic checkpoints. Nature Communications (2018).
4. The Insulin-Sensitizer Pioglitazone Remodels Adipose Tissue Phospholipids in Humans. Frontiers in Physiology (2021).
5. Nutritional load in post-prandial oxidative stress and the pathogeneses of diabetes mellitus. npj Science of Food (2024).
6. Impaired Remodeling of White Adipose Tissue in Obesity and Aging: From Defective Adipogenesis to Adipose Organ Dysfunction. Cells (2024).