Review: Ageing Adipose Tissue, Fat Redistribution and Metabolic Decline
This review links declining preadipocyte differentiation in ageing adipose tissue to hypertrophic lipid storage, fat redistribution toward visceral and other depots, and greater insulin resistance; it appraises proposed therapies ranked by translational readiness. [1]
Automatic summary · not editorially reviewed
The key findings
The review attributes the age-related adipogenic deficit to transcriptional reprogramming, SIRT7/SIRT1 and NAD dysregulation, nuclear lamina remodelling and senescent-cell inflammation. [1]
Fat redistributes from subcutaneous toward visceral, hepatic, muscular and perivascular depots, which the review links to insulin resistance, Type 2 diabetes and cardiovascular disease. [1]
Senolytics, NAD precursors and incretin-based agents are reviewed alongside still-preclinical stem cell and CRISPR approaches, ranked by translational readiness. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- Ageing adipose tissue and its progenitors, discussed in a review of human and rodent evidence
- Summary based on
- Study abstract
- Original publication
- June 28, 2026
Ageing depots: four interlocking defects
The review describes ageing adipose tissue through four interlocking defects. Transcriptional reprogramming, including induction of the inhibitory CCAAT/enhancer-binding protein β-LIP isoform via CUG triplet repeat-binding protein 1 and reduced C/EBPα and peroxisome proliferator-activated receptor γ activity, shifts progenitors away from differentiation toward hypertrophic lipid storage. SIRT7 opposes SIRT1 in regulating adipogenic commitment, implicating sirtuin and NAD dysregulation. Nuclear lamina remodelling restricts chromatin accessibility at adipogenic loci. Senescent cells accumulate and release a senescence-associated secretory phenotype enriched in interleukin-6, tumour necrosis factor-α and matrix metalloproteinases, sustaining local inflammation and inhibiting preadipocyte differentiation.
Supporting source [1]
Fat redistribution and metabolic outcomes in ageing
These changes occur alongside redistribution of fat from subcutaneous depots toward visceral, hepatic, muscular and perivascular compartments. The review states this redistribution accelerates insulin resistance, Type 2 diabetes and cardiovascular disease. Sex-specific depot trajectories diverge, and rodent models reproduce these patterns only partly. The review frames these as age-related associations and mechanisms, not as proven causes of disease in people.
Supporting source [1]
Proposed therapies ranked by translational readiness
The review appraises therapeutic strategies that may restore adipose progenitor competence or limit downstream metabolic dysfunction. It reviews senolytics, NAD precursors and incretin-based agents, including GLP-1 and dual GIP/GLP-1 receptor agonists, together with still-preclinical stem cell and CRISPR approaches, ranked by translational readiness. The conclusion suggests that restoring adipose progenitor competence while preserving depot-specific metabolic identity may help slow age-related metabolic deterioration and prolong healthspan. These are proposed strategies, not established treatments.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. It synthesizes mechanisms and proposed therapies rather than reporting a new study, and it notes that rodent models reproduce the patterns only partly. The therapeutic strategies are proposed, not established treatments.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Matar DB, Elahi MA, Nassar WK, Alotaibi MI, Murphy D, Fakhoury HMA, Aljada A. · europepmc.org · June 28, 2026