The DOI matches its Crossref record; 152 of the 154 references it cites were found in a registry or an index.
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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Citations
Cites
Positional cloning of the mouse obese gene and its human homologue
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994) · Nature · doi:10.1038/372425a0 · Cited by 13,419
Ng, M., Fleming, T., Robinson, M., Thomson, B., Graetz, N., Margono, C., Mullany, E. C., Biryukov, S., Abbafati, C., Abera, S. F., et al. (2014) · The Lancet · doi:10.1016/s0140-6736(14)60460-8 · Cited by 11,952
A New Initiative on Precision Medicine
Collins, F. S., & Varmus, H. (2015) · New England Journal of Medicine · doi:10.1056/nejmp1500523 · Cited by 5,202
Genetic studies of body mass index yield new insights for obesity biology
Study, T. L. C., Locke, A. E., The ADIPOGen Consortium, The AGEN-BMI Working Group, The CARDIOGRAMplusC4D Consortium, The CKDGen Consortium, The, G. L. G. C., The, I. C. B. P., The MAGIC Investigators, The MuTHER Consortium, et al. (2015) · Nature · doi:10.1038/nature14177 · Cited by 4,534
Self-citationFrayling, T. M., Timpson, N. J., Weedon, M. N., Zeggini, E., Freathy, R. M., Lindgren, C. M., Perry, J. R. B., Elliott, K. S., Lango, H., Rayner, N. W., et al. (2007) · Science · doi:10.1126/science.1141634 · Cited by 4,531
Abdominal obesity and metabolic syndrome
Després, J.-P., & Lemieux, I. (2006) · Nature · doi:10.1038/nature05488 · Cited by 4,354
CpG islands and the regulation of transcription
Deaton, A. M., & Bird, A. (2011) · Genes & Development · doi:10.1101/gad.2037511 · Cited by 3,187
Years of Life Lost Due to Obesity
Fontaine, K. R., Redden, D. T., Wang, C., Westfall, A. O., & Allison, D. B. (2003) · JAMA · doi:10.1001/jama.289.2.187 · Cited by 2,551
Yengo, L., Sidorenko, J., Kemper, K. E., Zheng, Z., Wood, A. R., Weedon, M. N., Frayling, T. M., Hirschhorn, J. N., Yang, J., & Visscher, P. M. (2018) · Human Molecular Genetics · doi:10.1093/hmg/ddy271 · Cited by 2,393
Effects of Recombinant Leptin Therapy in a Child with Congenital Leptin Deficiency
Farooqi, I. S., Jebb, S. A., Langmack, G., Lawrence, E., Cheetham, C. H., Prentice, A. M., Hughes, I. A., McCamish, M. A., & O'Rahilly, S. (1999) · New England Journal of Medicine · doi:10.1056/nejm199909163411204 · Cited by 1,998
Cited by
Sorted by citations
Obesity: global epidemiology and pathogenesis
Blüher, M. (2019) · Nature Reviews Endocrinology · doi:10.1038/s41574-019-0176-8 · Cited by 5,126
Self-citationEpigenetic regulation in metabolic diseases: mechanisms and advances in clinical study
Wu, Y., Lin, Z., Li, C., Lin, X. J., Shan, S., Guo, B., Zheng, M.-H., Li, F., Yuan, L., & Li, Z. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01333-7 · Cited by 549
Advantages and Limitations of the Body Mass Index (BMI) to Assess Adult Obesity
Wu, Y., Li, D., & Vermund, S. H. (2024) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph21060757 · Cited by 332
“However, the genetics of obesity are not sufficient to account for the variability of BMI [20,21].”
BackgroundWeight bias among health care professionals: A systematic review and meta‐analysis
Lawrence, B. J., Kerr, D., Pollard, C. M., Theophilus, M., Alexander, E., Haywood, D., & O’Connor, M. (2021) · Obesity · doi:10.1002/oby.23266 · Cited by 283
Arcuate Nucleus-Dependent Regulation of Metabolism—Pathways to Obesity and Diabetes Mellitus
Jaïs, A., & Brüning, J. C. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnab025 · Cited by 298
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
