Narrative review: nutrition, adipose tissue expandability and obesity-related metabolic risk
This narrative review proposes that limited capacity of white adipose tissue to store excess energy safely may drive lipid spillover, insulin resistance and metabolic disease, and uses bariatric surgery as a model of weight loss. [1]
Automatic summary · not editorially reviewed
The key findings
The review defines adipose tissue expandability as the capacity of white adipose tissue to store excess energy safely while preserving metabolic homeostasis, through more and larger adipocytes. [1]
When expandability is limited, the authors hypothesize that adipocyte hypertrophy predominates and triggers hypoxia, endoplasmic reticulum stress, chronic low-grade inflammation and fibrosis. [1]
Bariatric surgery is used as a physiological model showing that weight loss reduces lipid overflow while intrinsic adipose tissue expandability may remain incompletely restored. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- White adipose tissue and obesity-related metabolic disease, discussed conceptually; bariatric surgery used as a model
- Summary based on
- Study abstract
- Original publication
- September 20, 2026
Proposed framework of healthy versus limited fat storage
The review defines adipose tissue expandability as the capacity of white adipose tissue to store excess energy safely while preserving metabolic homeostasis. This adaptation is described as occurring through more adipocytes (hyperplasia) and larger adipocytes (hypertrophy). Healthy expansion is said to require coordinated angiogenesis, extracellular matrix remodeling and functional adipose stem and progenitor cells. When expandability is limited, for example by genetic factors, aging or chronic overnutrition, the authors propose that adipocyte hypertrophy predominates. They hypothesize that this triggers hypoxia, endoplasmic reticulum stress, chronic low-grade inflammation and fibrosis. These are presented as proposed mechanisms, not established causes.
Supporting source [1]
Proposed lipid spillover and insulin resistance pathways
According to the review, the proposed inflammatory and fibrotic changes could form a physical and metabolic barrier that compromises further safe lipid storage. Surplus lipids might then spill over to ectopic sites: the liver (promoting steatosis and hepatic insulin resistance), skeletal muscle (intramyocellular lipid accumulation and impaired glucose uptake) and pancreas (β-cell dysfunction and reduced insulin secretion). Lipotoxic intermediates such as diacylglycerols and ceramides are described as activating protein kinase C isoforms and possibly impairing insulin receptor signaling, thereby contributing to systemic insulin resistance. The clinical correlate is described as a spectrum of metabolic disorders including type 2 diabetes, dyslipidemia, metabolic dysfunction-associated steatotic liver disease and cardiovascular disease. These links are framed as hypotheses within a conceptual framework.
Supporting source [1]
Bariatric surgery as a model and review scope
The stated aim is to analyze how nutritional factors shape adipose tissue expandability and how limitations in expandability drive obesity-related metabolic disease. The authors use bariatric surgery as a physiological model illustrating how weight loss reduces lipid overflow, while intrinsic adipose tissue expandability may remain incompletely restored. They suggest that understanding determinants of expandability, from adipose stem cell function and angiogenesis to fibrosis and immune cell infiltration, could help identify individuals at risk despite normal body weight and support development of targeted therapies. This is a narrative review of a conceptual framework; the abstract reports no study design, sample, follow-up or measured outcomes, and the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a narrative review presenting a conceptual framework with hypothesized mechanisms, not a study with reported design, sample, follow-up or measured outcomes. Proposed pathways and clinical links are not established causal findings.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Jiménez-Flores E, Reytor-González C, Jima Gavilanes D, Rossetti G, Pilone V, Parrillo L, Cavallo M, Cobellis L, Simancas-Racines D, Schiavo L. · europepmc.org · September 20, 2026