Obesity–a genetic disease of adipose tissue?
Open accessAbstract
Although the rapid increase in the prevalence of obesity in many countries suggests that environmental factors (mainly overeating and physical inactivity) play the most important role in the development of overweight, it is very likely that genetic factors also contribute. It appears that one major gene in combination with one or several minor genes constitute the genetic components behind excess accumulation of body fat in most obese individuals. However, monogenic obesity has been described in a few families due to changes in leptin, leptin receptor, prohormone convertase, pro-opiomelanocortin or melanocortin-4 receptor. None of the monogenic variants is of great importance for common human obesity; the latter genes are unknown so far. Results from genomic scans suggest that major obesity genes are located on chromosomes 2, 10, 11 and 20. Studies of candidate genes indicate that the minor obesity genes control important functions of adipose tissue, and that structural variance in these genes may alter adipose tissue function in a way that promotes obesity. Such genes are beta 2- and beta 3-adrenoceptors, hormone-sensitive lipase, tumour necrosis factor alpha, uncoupling protein-1, low-density lipoprotein receptor, and peroxisome proliferator activator receptor gamma-2. Some of these genes may promote obesity by gene-gene interactions (for example beta 3-adrenoceptors and uncoupling protein-1) or gene-environment interactions (for example beta 2-adrenoceptors and physical activity). Some are important for obesity only among women (for example beta 2- and beta 3-adrenoceptors, low-density lipoprotein receptor and tumour necrosis factor alpha). Few 'non-adipose' genes have so far shown a firm association to common human obesity, which could suggest that the important genes for the development of excess body fat also control adipose tissue function.
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This remodeling is characterized by changes such as modification of adipocyte area, disturbance in fatty acid turnover, rearrangement of extracellular matrix components, inflammation, and modulation of the browning phenotype.
“This process is characterized by a set of changes, such as: modification of the adipocyte area (hypertrophy, hyperplasia or atrophy; Arner, 2000); disturbance in fatty acid turnover (lipolysis and lipogenesis; Arner et al., 2010); rearrangement of extra-cellular matrix components (Scherer, 2016); inflammation (Batista et al., 2012); modulation of the browning phenotype related to the thermogenic”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Arner, 2000
The Arner (2000) citation is attached specifically to changes in adipocyte area—hypertrophy, hyperplasia or atrophy—not to the other changes in the sentence. The PPARγ-2 section discusses adipocyte differentiation and development of fat mass, but the passages found for adipocyte size, hypertrophy and hyperplasia do not address the cited claim about changes in adipocyte area. (LLM, conf=0.70)
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- Authors
- Arner, P.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Arner, Peter
- ORCID
- Arner, Peter
- Venue
- British Journal Of Nutrition
- Publisher
- Cambridge University Press (CUP)
- Published
- 2000-06
- Volume
- 83
- Issue
- S1
- Pages
- S9-S16
- ISSN
- 0007-1145 (ISSN-L)
- 1475-2662
- OpenAlex
- W2001398343
- Cited by
- 84
- References
- 85
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 1 · 2015: 5 · 2012: 4
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal Of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- obesity, genetic susceptibility, adipose tissue function, monogenic obesity, leptin, leptin receptor, prohormone convertases, proopiomelanocortin, melanocortin-4 receptor, candidate genes, gene-gene interaction, gene-environment interaction, beta2-adrenergic receptor, beta-3 adrenoceptor, UCP1, TNF-α, LDL receptor, hormone-sensitive lipase, sex differences in obesity, body fat accumulation
- MeSH terms
- Uncoupling Protein 1, Adipose Tissue, Body Temperature Regulation, Carrier Proteins, Sterol Esterase, Connective Tissue Diseases, Female, Humans, Ion Channels, Male, Membrane Proteins, Obesity, Polymorphism, Genetic, Receptors, Adrenergic, beta, Receptors, LDL, Sex Factors, Transcription Factors, Tumor Necrosis Factor-alpha, Body Mass Index, Receptors, Cytoplasmic and Nuclear, Mitochondrial Proteins
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