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Adipose tissue expandability, lipotoxicity and the Metabolic Syndrome — An allostatic perspective
Abstract
While the link between obesity and type 2 diabetes is clear on an epidemiological level, the underlying mechanism linking these two common disorders is not as clearly understood. One hypothesis linking obesity to type 2 diabetes is the adipose tissue expandability hypothesis. The adipose tissue expandability hypothesis states that a failure in the capacity for adipose tissue expansion, rather than obesity per se is the key factor linking positive energy balance and type 2 diabetes. All individuals possess a maximum capacity for adipose expansion which is determined by both genetic and environmental factors. Once the adipose tissue expansion limit is reached, adipose tissue ceases to store energy efficiently and lipids begin to accumulate in other tissues. Ectopic lipid accumulation in non-adipocyte cells causes lipotoxic insults including insulin resistance, apoptosis and inflammation. This article discusses the links between adipokines, inflammation, adipose tissue expandability and lipotoxicity. Finally, we will discuss how considering the concept of allostasis may enable a better understanding of how diabetes develops and allow the rational design of new anti diabetic treatments.
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“Evidence suggests that dysfunctional AT promotes systemic low-grade inflammation, fat overflow, and, hence, ectopic lipid deposition, which further contributes to insulin resistance (Virtue and Vidal-Puig, 2010).”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Virtue and Vidal-Puig, 2010
In the citing paper
“Excessive abdominal fat is associated with adipose tissue dysfunction, leading to systemic low-grade inflammation, fat overflow, ectopic lipid deposition, and reduced insulin sensitivity.”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Virtue and Vidal-Puig, 2010
In the citing paper
“In fact, under excess caloric intake, WAT reaches its upper limit for further lipid storage ([157](#B157), [169](#B169)).”
From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [169]
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Metadata
- Authors
- Virtue, S., & Vidal-Puig, A.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Virtue, Sam
- ORCID
- Virtue, Sam
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 1801
- Issue
- 3
- Pages
- 338-349
- ISSN
- 1388-1981 (ISSN-L)
- OpenAlex
- W2035489548
- Semantic Scholar
- 470ac3b56b5b657fa79061f68dcdb8d8593fc4e8
- Cited by
- 1,013
- References
- 80
- Citations by year
- 2026: 58 · 2025: 65 · 2024: 49 · 2023: 46 · 2022: 68 · 2021: 62 · 2020: 52 · 2019: 68 · 2018: 77 · 2017: 75 · 2016: 64 · 2015: 66 · 2014: 68 · 2013: 76 · 2012: 69
- FWCI
- 6.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Diabetes UK
- Medical Research Council
- Biotechnology and Biological Sciences Research Council (BB/E011950/1)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- adipose tissue expandability, lipotoxicity, metabolic syndrome, obesity, type 2 diabetes, allostasis, ectopic fat deposition, insulin resistance, adipokines, inflammation, apoptosis, diabetes treatment
- MeSH terms
- Adipose Tissue, Animals, Cell Differentiation, Diabetes Mellitus, Humans, Insulin Resistance, Liver, Models, Biological, Neovascularization, Pathologic, Adipocytes, Metabolic Syndrome, Lipid Metabolism, Insulin-Secreting Cells, Allostasis
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