ArticleJACC. Basic to translational science2026
Rethinking Obesity Through the Lens of Lipid Spillover.
Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- SGLT2 inhibitors are associated with reductions in epicardial adipose tissue volume and thickness: a meta-analysis.International journal of obesity (2005) · 2026Pooled it
- Preoperative Magnetic Resonance Imaging-Derived Adiposity Profiling and Cardiometabolic Remodeling After Metabolic and Bariatric Surgery.Obesity surgery · 2026Article
- Reply to 'Bedside epicardial adipose tissue assessment in the era of advanced adipose phenotyping'.Nature reviews. Cardiology · 2026Article
- Composite metabolic biomarkers for cardiovascular risk assessment in CKM syndrome.Cardiovascular diabetology · 2026Article
- Rethinking cardiometabolic therapy thresholds in individuals with obesity.International journal of obesity (2005) · 2026Review
- Role of systemic and epicardial adipose tissue in cardiometabolic disease.Nature reviews. Cardiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conventional models frame obesity as excess caloric intake but do not explain why cardiometabolic disease develops in only a subset of individuals. Building on Unger's seminal lipotoxicity hypothesis and subsequent adipose expandability frameworks, the lipid spillover concept emphasizes adipose tissue dysfunction-rather than total fat mass-as the driver of disease. When subcutaneous adipose tissue reaches its safe storage capacity, adipocyte hypertrophy, inflammation, and insulin resistance increase lipolysis, raising circulating free fatty acids and promoting ectopic lipid deposition. Accumulation of fat in organs such as the liver, heart, skeletal muscle, pancreas, vasculature, and kidneys initiates organ-specific injury and systemic metabolic-vascular dysfunction that may occur independently of body mass index. Visceral, perivascular, and epicardial fat depots act as inflammatory reservoirs that exacerbate vascular disease and myocardial dysfunction. Advances in imaging and biomarker profiling now enable quantification of ectopic fat burden and activity, supporting risk stratification beyond body size alone. Therapeutic strategies that preferentially reduce ectopic fat through lifestyle intervention, pharmacotherapy, or bariatric surgery, offer targeted cardiometabolic risk reduction.
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Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.