Unraveling the Genetics of Human Obesity
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The use of modern molecular biology tools in deciphering the perturbed biochemistry and physiology underlying the obese state has proven invaluable. Identifying the hypothalamic leptin/melanocortin pathway as critical in many cases of monogenic obesity has permitted targeted, hypothesis-driven experiments to be performed, and has implicated new candidates as causative for previously uncharacterized clinical cases of obesity. Meanwhile, the effects of mutations in the melanocortin-4 receptor gene, for which the obese phenotype varies in the degree of severity among individuals, are now thought to be influenced by one's environmental surroundings. Molecular approaches have revealed that syndromes (Prader-Willi and Bardet-Biedl) previously assumed to be controlled by a single gene are, conversely, regulated by multiple elements. Finally, the application of comprehensive profiling technologies coupled with creative statistical analyses has revealed that interactions between genetic and environmental factors are responsible for the common obesity currently challenging many Westernized societies. As such, an improved understanding of the different "types" of obesity not only permits the development of potential therapies, but also proposes novel and often unexpected directions in deciphering the dysfunctional state of obesity.
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In the initial phase, behavioral and environmental factors could play a key role in the constitution of adipose tissue excess on a genetically predisposed background.
“In the initial phase, behavioral and environmental factors could play a key role in the constitution of adipose tissue excess on a genetically predisposed background [61].”
From Adipose tissue transcriptomic signature highlights the pathological relevance of extracellular matrix in human obesity (2008) · cites this paper as [61]
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- Authors
- Mutch, D. M., & Clément, K.
- Affiliations
- Inserm (FR)
- University College London (GB)
- Corresponding author
- Clément, Karine
- Venue
- PLoS Genetics
- Publisher
- Public Library of Science (PLoS)
- Published
- 2006
- Volume
- 2
- Issue
- 12
- Pages
- e188
- ISSN
- 1553-7390 (ISSN-L)
- 1553-7404
- PMC
- PMC1756898
- OpenAlex
- W1977583120
- Cited by
- 169
- References
- 74
- Citations by year
- 2026: 1 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 6 · 2019: 8 · 2018: 7 · 2017: 10 · 2016: 12 · 2015: 7 · 2014: 11 · 2013: 13 · 2012: 13
- FWCI
- 1.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Genetics (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- human obesity, monogenic obesity, leptin, melanocortin pathway, melanocortin-4 receptor, Prader-Willi syndrome, Bardet-Biedl syndrome, gene-environment interaction, obesity phenotypes, obesity treatment
- MeSH terms
- Animals, Chromosome Mapping, Environment, Humans, Hypothalamus, Mutation, Obesity, Phenotype, Syndrome, Gene Expression Profiling
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