What causes the insulin resistance underlying obesity?
Open accessAbstract
PURPOSE OF REVIEW: The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts. RECENT FINDINGS: The specific link between visceral adipose tissue accumulation and insulin resistance continues to be discerned. Visceral adiposity is correlated with accumulation of excess lipid in liver, and results in cell autonomous impairment in insulin signaling. Visceral adipose tissue is also prone to inflammation and inflammatory cytokine production, which also contribute to impairment in insulin signaling. The expansion of visceral adipose tissue and excess lipid accumulation in liver and muscle may result from limited expandability of subcutaneous adipose tissue, due to the properties of its extracellular matrix and capacity for capillary growth. SUMMARY: Recent studies underscore the need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the mechanisms by which the size of adipose tissue depots is determined.
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It has been hypothesized that once the genetically determined limit of expandability of SAT is reached, there is expansion of VAT and excess lipid accumulation in muscle, liver and other organs, resulting in insulin resistance, inflammation and metabolic dysregulation.
“It has been hypothesized that once the genetically determined limit of expandability of SAT is reached, there is expansion of VAT and excess lipid accumulation in muscle, liver and other organs, resulting in IR, inflammation and metabolic dysregulation [151].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [151]
The ‘Adipose tissue expandability and protection from insulin resistance’ section (page not available) links limited fat-storage capacity to lipid deposition in visceral adipose tissue, liver and muscle, and to insulin resistance. The paper also discusses visceral inflammation. It does not describe the limit of subcutaneous adipose tissue expandability as genetically determined; it says the mechanisms determining expandability are not known. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn humans, there is large individual variation in the fat storage capability and expandability of different adipose tissue depots.
“In humans, there is large individual variation in the fat storage capability and expandability of different adipose tissue depots [151].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [151]
Excess accumulation of SAT is much less likely to cause insulin resistance and metabolic dysfunction and explains why IR is not observed in all obese individuals.
“In addition, excess accumulation of SAT is much less likely to cause IR and metabolic dysfunction and explains why IR is not observed in all obese individuals [151,181].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [151]
It has been firmly established that T2D is caused by the dysfunctional exocrine function of the pancreas, and peripheral insulin resistance is a requisite precursor for the development of this disease.
“It has been firmly established that T2D is caused by the dysfunctional exocrine function of the pancreas, and peripheral insulin resistance is a requisite precursor for the development of this disease.105,112”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [112]
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“It has been hypothesised that once the genetically determined limit of expandability of SAT is reached, there is expansion of VAT and excess lipid accumulation in muscle, liver and other organs, resulting in IR, inflammation and metabolic dysregulation (150).”
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“Additionally, insulin resistance impairs the body’s ability to utilize glucose effectively, promoting fat accumulation [138,139].”
- Authors
- Hardy, O. T., Czech, M. P., & Corvera, S.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Corvera, Silvia
- Venue
- Current Opinion in Endocrinology, Diabetes & Obesity
- Published
- 2012-04
- Volume
- 19
- Issue
- 2
- Pages
- 81-87
- ISSN
- 1752-296X (ISSN-L)
- PMC
- PMC4038351
- OpenAlex
- W2101510325
- Cited by
- 563
- References
- 49
- Citations by year
- 2026: 29 · 2025: 49 · 2024: 55 · 2023: 44 · 2022: 59 · 2021: 65 · 2020: 56 · 2019: 45 · 2018: 36 · 2017: 32 · 2016: 24 · 2015: 20 · 2014: 19 · 2013: 22 · 2012: 8
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Endocrinology Diabetes and Obesity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship@UMassChan (submittedVersion)
- Funders
- University of Massachusetts
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK030898, R01DK089101, R37DK030898, DK30898, DK089101)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- insulin resistance, obesity, visceral adipose tissue, ectopic fat deposition, hepatic lipid accumulation, muscle lipid accumulation, insulin signaling, adipose tissue inflammation, inflammatory cytokines, extracellular matrix, adipose tissue depots
- MeSH terms
- Diabetes Mellitus, Type 2, Fatty Liver, Female, Humans, Insulin Resistance, Male, Obesity, Intra-Abdominal Fat
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