Metabolic disorders articles from across Nature Portfolio

Wang Lin and his colleagues explore how aging reprograms spatially unique pathways in liver endothelial cells to cause fibrosis. They find that loss of KIT in liver endothelial cells close to the central vein upregulates the chemokine receptor CXCR4 to stimulate inflammation, enhance fibrosis and increase lipid accumulation in aged liver.

Some individuals with obesity have a healthy metabolic profile and are not at increased risk for diabetes or cardiovascular disease. The mechanisms behind this phenomenon are poorly understood, but recent work now characterizes the biological underpinnings of the metabolically healthy obese phenotype.

A major challenge in human genetics is the prioritization of causal genes in common complex diseases. A genome-wide CRISPR screen for intracellular insulin content in a human β-cell line has now identified a new candidate gene for type 2 diabetes, demonstrating the utility of this screening approach in β-cells.

Aging is known to exacerbate atherosclerosis, but the mechanisms have been largely unknown. A study in Nature Aging reveals a bone-marrow-controlled axis of clonality during atherosclerosis, showing that aged bones drive an inflammatory milieu that promotes smooth muscle polyclonality and the formation of larger lesions.