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Genetics and epigenetics in obesity
Open accessAbstract
Obesity is among the most threatening health burdens worldwide and its prevalence has markedly increased over the last decades. Obesity maybe considered a heritable trait. Identifications of rare cases of monogenic obesity unveiled that hypothalamic circuits and the brain-adipose axis play an important role in the regulation of energy homeostasis, appetite, hunger and satiety. For example, mutations in the leptin gene cause obesity through almost unsuppressed overeating. Common (multifactorial) obesity, most likely resulting from a concerted interplay of genetic, epigenetic and environmental factors, is clearly linked to genetic predisposition by multiple risk variants, which, however only account for a minor part of the general BMI variability. Although GWAS opened new avenues in elucidating the complex genetics behind common obesity, understanding the biological mechanisms relative to the specific risk contributing to obesity remains poorly understood. Non-genetic factors such as eating behavior or physical activity strongly modulate the individual risk for developing obesity. These factors may interact with genetic predisposition for obesity through epigenetic mechanisms. Thus, here, we review the current knowledge about monogenic and common (multifactorial) obesity highlighting the important recent advances in our knowledge on how epigenetic regulation is involved in the etiology of obesity.
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“However, the genetics of obesity are not sufficient to account for the variability of BMI [20,21].”
From Advantages and Limitations of the Body Mass Index (BMI) to Assess Adult Obesity (2024) · cites this paper as [20]
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Metadata
- Authors
- Rohde, K., Keller, M., la Cour Poulsen, L., Blüher, M., Kovacs, P., & Böttcher, Y.
- Affiliations
- University of Oslo (NO)
- IFB Adiposity Diseases (DE)
- Leipzig University (DE)
- Corresponding author
- Rohde, Kerstin
- Keller, Maria
- Blüher, Matthias
- Kovacs, Peter
- Böttcher, Yvonne
- Venue
- Metabolism
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 92
- Pages
- 37-50
- ISSN
- 0026-0495 (ISSN-L)
- OpenAlex
- W2898859410
- Cited by
- 355
- References
- 154
- Citations by year
- 2026: 13 · 2025: 43 · 2024: 38 · 2023: 52 · 2022: 61 · 2021: 82 · 2020: 45 · 2019: 21
- FWCI
- 5.21
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-nd
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- Locations
- Metabolism (publishedVersion)
- PubMed (publishedVersion)
- NORA - Norwegian Open Research Archives (submittedVersion, cc-by-nc-nd)
- Funders
- BMBF (FKZ: 01EO1501)
- European Union Seventh Framework Programme (FP7-PEOPLE-2013-COFUND)
- Helse Sør-Øst
- Deutsche Forschungsgemeinschaft
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Keywords
- obesity, monogenic obesity, epigenetics, genetic susceptibility, leptin, hypothalamic circuits, energy homeostasis, appetite and satiety, genetic risk variants, dietary habits, physical activity, gene-environment interaction
- MeSH terms
- Humans, Obesity, Genetic Predisposition to Disease, Epigenesis, Genetic, Precision Medicine
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