The DOI matches its Crossref record; 264 of the 264 references it cites were found in a registry or an index.
Adipose tissue hyperplasia and hypertrophy in common and syndromic obesity-the case of BBS obesity
Open accessAbstract
Obesity is a metabolic state generated by the expansion of adipose tissue. Adipose tissue expansion depends on the interplay between hyperplasia and hypertrophy, and is mainly regulated by a complex interaction between genetics and excess energy intake. However, the genetic regulation of adipose tissue expansion is yet to be fully understood. Obesity can be divided into common multifactorial/polygenic obesity and monogenic obesity, non-syndromic and syndromic. Several genes related to obesity were found through studies of monogenic non-syndromic obesity models. However, syndromic obesity, characterized by additional features other than obesity, suggesting a more global role of the mutant genes related to the syndrome and, thus, an additional peripheral influence on the development of obesity, were hardly studied to date in this regard. This review summarizes present knowledge regarding the hyperplasia and hypertrophy of adipocytes in common obesity. Additionally, we highlight the scarce research on syndromic obesity as a model for studying adipocyte hyperplasia and hypertrophy, focusing on Bardet–Biedl syndrome (BBS). BBS obesity involves central and peripheral mechanisms, with molecular and mechanistic alternation in adipocyte hyperplasia and hypertrophy. Thus, we argue that using syndromic obesity models, such as BBS, can further advance our knowledge regarding peripheral adipocyte regulation in obesity.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Hyperplasia and hypertrophy can occur in a depot-specific manner, as intra-abdominal fat depots primarily expand through hypertrophy, while subcutaneous WAT has been seen to expand through both methods (54).”
From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [54]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The metabolic phenotype in obesity: Fat mass, body fat distribution, and adipose tissue function
Goossens, G. H. (2017) · Obesity Facts · doi:10.1159/000471488 · Cited by 8,481
Genetics of Food Intake Self-Regulation in Childhood: Literature Review and Research Opportunities
Faith, M. S., Carnell, S., & Kral, T. V. E. (2013) · Human Heredity · doi:10.1159/000353879 · Cited by 7,633
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
Mechanisms of fatty acid-induced inhibition of glucose uptake.
Boden, G., Chen, X., Ruiz, J., White, J. V., & Rossetti, L. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117252 · Cited by 3,720
Targeted disruption of the melanocortin-4 receptor results in obesity in mice
Huszar, D., Lynch, C. A., Fairchild-Huntress, V., Dunmore, J. H., Fang, Q., Berkemeier, L. R., Gu, W., Kesterson, R. A., Boston, B. A., Cone, R. D., et al. (1997) · Cell · doi:10.1016/s0092-8674(00)81865-6 · Cited by 3,030
Pathophysiology of human visceral obesity: an update
Tchernof, A., & Després, J.-P. (2013) · Physiological Reviews · doi:10.1152/physrev.00033.2011 · Cited by 2,583
What we talk about when we talk about fat
Rosen, E. D., & Spiegelman, B. M. (2014) · Cell · doi:10.1016/j.cell.2013.12.012 · Cited by 2,373
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 2,368
Dynamics of fat cell turnover in humans
Spalding, K. L., Arner, E., Westermark, P. O., Bernard, S., Buchholz, B. A., Bergmann, O., Blomqvist, L., Hoffstedt, J., Näslund, E., Britton, T., et al. (2008) · Nature · doi:10.1038/nature06902 · Cited by 2,357 · cited 4×
“However, shown by several elegant studies, at any life stage, states of over-nutrition lead to adipose tissue hyperplasia and, consequently, to an increased mass [14,50,51,59].”
BackgroundInfluentialmPPAR gamma 2: tissue-specific regulator of an adipocyte enhancer.Preprint
Tontonoz, P., Hu, E., Graves, R. A., Budavari, A. I., & Spiegelman, B. M. (1994) · Genes & Development · doi:10.1101/gad.8.10.1224 · Cited by 2,181
Flagged first, then by citations
Research works printed but not linked: 1
- Macdougald, O.A. (2014). Methods in Enzymology, Academic Press. [1st ed.].
Cited by
Sorted by citations
Items 101–143 of 143
Epidemiology and Pathophysiology of Malnutrition and Obesity
Mannan, A., Sharma, A., & Singh, T. G. (2025) · Springer eBooks · doi:10.1007/978-981-95-2994-0_17
Azar, F. A., Vivoli, A., Machuca‐Parra, A. I., Paré, F., Civelek, M., Shou, W., & Lim, G. E. (2025) · Physiological Reports · doi:10.14814/phy2.70681
“…that the number of adipocytes in humans remains stable throughout adulthood, with marginal changes in adipocyte turnover (Haczeyni et al., 2018; Horwitz & Birk, 2023; Spalding et al., 2008; White, 2023), but as individuals with obesity tend to have more adipocytes compared to leaner…”
Leebana, M., & Prathyusha., P. (2025) · Oriental Journal Of Chemistry · doi:10.13005/ojc/410621
Stafeev, I., & Parfyonova, Y. E. (2026) · Diabetes Mellitus · doi:10.14341/dm13331
“Классическим и наиболее распространенным в мире примером является гипер-функциональное состояние жировой ткани, именуемое ожирением [2].”
Cellular Cytokine Storm-Mediated Inflammation in Metabolic Disorders
Bandyopadhyay, B., Sasmal, S., Kanrar, A., & Adhikary, S. (2026) · Springer eBooks · doi:10.1007/978-3-032-11752-6_8
Panx1 deficiency exacerbates GAN diet-induced obesity by destabilizing β-catenin via GSK3β
Xu, H., Zhao, J., Lu, S., Wang, Q., Sun, R., Gao, Y., Xie, F., Wang, Y., Cao, R., Feng, Y., et al. (2026) · iScience · doi:10.1016/j.isci.2026.115098
“7 Pannexin 1 (Panx1) is a channel-forming glycoprotein belonging to the innexin family.”
The evolution of obesity pharmacotherapy from sympathomimetics to incretin-based therapies
Ncube, K. N., Moloi, N., & Malange, T. D. (2026) · SA pharmaceutical journal. · doi:10.36303/sapj.4108
Yuri, G., Santillana, N., Soto, L., Pereira, A., Corvalán, C., & Cifuentes, M. (2026) · Journal of Obesity · doi:10.1155/jobe/5233463
Woramongkolchai, N., Chaotham, C., Suriya, U., Khine, H. E. E., Poungcho, P., Ariyachet, C., Yen, C.-H., & Chansriniyom, C. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27093914
“Increases in the number and size of adipocytes, respectively known as adipocyte hyperplasia and hypertrophy, are influenced by insulin-mediated glucose uptake, de novo lipogenesis, and fatty acid uptake [3,4].”
Ancestry-informative regulatory variants at KCNB1 modulate adipogenesis and body mass index
Teixeira, S. K., Laurindo, C. P., Sato, F. T., Zuleta, L. F., Duarte, N., Jensen, A. V. V., Paço, S., Pereira, A. C., Sakabe, N., Nóbrega, M., et al. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1805824
“However, the mechanisms by which rs149309426 modulates KCNB1 expression outside adipose tissue remain unknown and warrant further investigation (58, 59).”
Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects
Na’aim, A. A., Kamarudin, T. A., Arshad, N. ‘., Za'aba, N. F., Kamaruddin, N. A., & Ahmad, F. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27114778
“…earlier studies proposed that adipose tissue expansion in adulthood occurs exclusively through hypertrophy, recent rodent lineage-tracing studies demonstrate that preadipocytes can also differentiate into new adipocytes, thereby contributing to adipose tissue expansion via hyperplasia [8,73,74].”
Electrochemical biosensor (OBSense) to detect childhood obesity: an in-vitro exploratory study
Hernandez-Reyes, M., Paramasivan, M., George, H., Mathew, J., Sun, Y., Wu, J., Yan, Y., Zhan, W., Mahmoud, A. M., Pesavento, R. P., et al. (2026) · Journal of Applied Electrochemistry · doi:10.1007/s10800-026-02501-7
Pädiatrische Diabetologie: Typ-2-Diabetes bei Kindern und Jugendlichen
Müssig, K., Karges, B., Bitzer, B., & Reinehr, T. (2026) · Deutsches Ärzteblatt · doi:10.3238/persdia.2026.06.26.01
AlSedairy, S. A., Subash‐Babu, P., Alhussain, M. H., Binobead, M. A., & Alshatwi, A. A. (2026) · ChemistryOpen · doi:10.1002/open.70230
“Hypertrophic adipocytes are linked to metabolic imbalance, insulin resistance, and inflammation during obe‐ sity, which is a result of an abnormal accumulation of lipids in adipocytes, causing them to become larger and resulting in the malfunctioning of adipose tissue [20].”
The Role of Angiogenesis in Breast Cancer and Obesity: Unravelling the Connection
Sikuza, Y. O. K., Basson, C., Oberholzer, N., & Ambele, M. A. (2026) · International Journal of Breast Cancer · doi:10.1155/ijbc/2364200 · Cited by 1
“On a cellular level, obesity is characterised by adipocyte expansion, which can either manifest as hypertrophy or hyperplasia [27].”
Suwannasual, U., & Lund, A. K. (2026) · Toxicology Reports · doi:10.1016/j.toxrep.2026.102304
“Importantly, increased adipocyte size (hypertrophy) in white adipose tissue is associated with higher levels of inflammation and increased insulin resistance when compared to hyperplasia of adipocytes during adipose remodeling [55].”
Vratarić, M., Alempijević, I., Bursać, B. N., Teofilović, A., Milutinović, D. V., & Djordjevic, A. D. (2026) · Journal of Endocrinological Investigation · doi:10.1007/s40618-026-02938-9
Chen, S., Yoon, J.-S., Park, E., Li, C., Ginting, R. P., LEE, M., Chau, G. C., Kim, M.-H., Hahn, M., Um, S. H., et al. (2026) · Cell Death and Differentiation · doi:10.1038/s41418-026-01799-2
Li, J., Wang, Y., Liu, C., Yuan, X., Sun, J., & Ji, H. (2026) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2026.111595
Early-life body mass index and adult fat distribution: a life-course Mendelian randomisation study
Lai, Q., Wang, Y., Wang, X., Ma, G., Yang, B., Song, J., & Gao, J. (2026) · BMJ Open · doi:10.1136/bmjopen-2026-122110
Chen, H.-R., Sun, B., Qiu, Y.-J., Hua, C., Lin, X.-X., & Gao, W. (2026) · Advancement of science · doi:10.1002/advs.76699
“This aligned with emerging evidence that dysregulated transcription factors in stromal cells contribute to adipose tissue remodeling in various hyperplastic and hypertrophic conditions [ 49, 50 ].”
Understanding adipocyte heterogeneity across species, depot, and disease
Kitto, E. S., Kult, S., & Emont, M. P. (2026) · Biochemical Society Transactions · doi:10.1042/bst20250327 · Cited by 1
“By contrast, a hyperplasic morphology (more numerous but smaller adipocytes) is generally linked to a more favorable metabolic profile, even at similar levels of total fat mass [36,37].”
Ortega, M. P. C., Peña-Peña, M., Carbó, R., Medina-Urrutia, A. X., Osorio‐Alonso, H., Jiang, B., Almanza-Pérez, J. C., Blancas‐Flores, G., Villafaña, S., Romero‐Nava, R., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27156693
“WAT hyperplasia is a process modulated by insulin, insulin-like growth factor 1 (IGF-1), and fibroblast growth factor 1 (FGF-1) [45].”
InfluentialGarcía-Carrillo, E., Pezoa-Fuentes, P., Guzmán-Muñoz, E., Concha‐Cisternas, Y., Montalva-Valenzuela, F., Arancibia, J. E. O., Aroca, J. G., Cortés-Roco, G., & Sepulveda, R. A. Y. (2026) · Journal of Clinical Medicine · doi:10.3390/jcm15156006 · Cited by 1
“From a biological perspective, excess adiposity is not metabolically inert; the pathological expansion of adipose tissue through hypertrophy and hyperplasia promotes the secretion of adipokines, cytokines, and chemokines with systemic effects on metabolism, inflammation, and organ function [3,4].”
Castro-Ribeiro, C., Azevedo, T., Barros, L., Silva‐Reis, R., Gonçalves, M., Ferreira, T., Ferreira, J. P. R. R., Ferreira, R. M., Martins, T., Pires, M. J., et al. (2026) · Current Issues in Molecular Biology · doi:10.3390/cimb48080797
“Under conditions of nutritional excess, adipose tissue expands through adipocyte hypertrophy and hyperplasia and undergoes functional remodeling that influences lipid metabolism, inflammatory response, and endocrine signaling [13].”
Li, H., Tang, L., Yuan, X., Ren, Z., Wei, M., Tian, Z., Xue, R., Gao, Z., Liu, C., Ji, H., et al. (2026) · Animal nutrition · doi:10.1016/j.aninu.2026.03.013
Zhai, C., Liu, Y., Li, X., Fang, X., & Liu, B. (2026) · Food Bioscience · doi:10.1016/j.fbio.2026.109725
The adipose organ–capacitor model of preclinical and clinical obesity
Nisoli, E. (2026) · Trends Open · doi:10.1016/j.treopn.2026.07.013
Azlan, A. H. M., Subramaniyan, V., Ong, L. C., Dawe, G. S., & Ravi, R. N. (2026) · Obesity Medicine · doi:10.1016/j.obmed.2026.100741
Ulusu, N. N. (2026) · Antioxidants · doi:10.3390/antiox15091143 · Cited by 1
“Beyond genetic and dietary drivers of adipocyte hypertrophy and hyperplasia, syndromic obesity models offer unique insights into the peripheral mechanisms regulating adipose tissue remodelling [50].”
New avenues in metabolic disease treatment: duodenal mucosal resurfacing and gene therapy
Dias, C., Patel, S., Gaglani, T., & Thosani, N. C. (2026) · Exploration of Endocrine and Metabolic Diseases · doi:10.37349/eemd.2026.101482
Pädiatrische Diabetologie: Typ-2-Diabetes bei Kindern und Jugendlichen
Müssig, K., Karges, B., Bitzer, B., & Reinehr, T. (2026) · Deutsches Ärzteblatt · doi:10.3238/perspaed.2026.10.02.01
A Twist in the Tale: Rare Diagnosis of Lipomatosis of the Appendix
Aini, D., Markovic, N., Rienzo, E., Topilow, A. A., & Parker, G. (2026) · Case Reports in Surgery · doi:10.1155/cris/5436727
Heart and Brain: Linking Obesity-Related Inflammation, Cardiovascular Disease and Cognitive Function
Reiss, A. B., Gulkarov, S., Syed, U., Ben-Dor, G. A., Srivastava, A., Singh, M., & Leon, J. D. (2026) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd13100477
Stanciu, D. I., Hudiță, A., Ginghină, O., & Gălățeanu, B. (2026) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2026.168488
Erkan, İ. B. Ö., Senturk, L. M., Erel, C. T., Seyisoğlu, H., Şahmay, S., & Durmuşoğlu, F. (2026) · Climacteric · doi:10.1080/13697137.2026.2735765
Samra, N. A., Suliman, S. G. I., Al-Hadad, M., Boomsma, D. I., Alhantoobi, F., AlSamahi, M. E., Abufarajallah, H., Tikriti, A. A., Aung, Z., Richards, S. E., et al. (2026) · Obesity Reviews · doi:10.1111/obr.70226
Karunarathne, W. A. H. M., Sanjaya, S. S., Park, S.-R., Choi, Y. H., Lee, C. S., & Kim, G.-Y. (2026) · Journal of Agriculture and Food Research · doi:10.1016/j.jafr.2026.103390
Metaflammation: linking diet and obesity to multiorgan dysfunction
Vieira, T. A., Cruzeiro, J., Grandini, N. A., Tanganini, M. D., dos Santos, M. D. P. S., Belin, M. A. F., Francisqueti‐Ferron, F. V., Ferron, A. J. T., & Corrêa, C. R. (2026) · Nutrire · doi:10.1186/s41110-026-00558-0
“Both hyperplasia and hypertrophy are important mechanisms for the expansion of adipose tissue and the storage of excess fat [ 31].”
InfluentialCavalcante, H. C., de Souza, D. M., Dutra, M. L. D. V., Fonte, M. B. B., D’Oliveira, A. B., Batista, K. S., de Oliveira, G. C., de Lima, R. L. F. C., Carvalho, L. R. R. A., de Araújo, A. N. V., et al. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2026.1933559
Shi, H., Sieusahai, J., Kamel, M., Wong, C. K. W., Mason, A., Younossi, Z. M., Corpechot, C., Grunvald, E. L., Troshyn, O., Galli, A., et al. (2026) · Nutrients · doi:10.3390/nu18213592
Metadata
- Authors
- Horwitz, A., & Birk, R.
- Affiliations
- Ariel University (IL)
- Corresponding author
- Birk, Ruth
- ORCID
- Birk, Ruth
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2023-08-04
- Volume
- 15
- Issue
- 15
- Pages
- 3445
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC10421039
- OpenAlex
- W4385577907
- Cited by
- 143
- References
- 264
- Citations by year
- 2026: 50 · 2025: 52 · 2024: 37 · 2023: 4
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- adipose tissue hyperplasia, adipocyte hypertrophy, syndromic obesity, Bardet-Biedl syndrome, monogenic obesity, polygenic obesity
- MeSH terms
- Adipose Tissue, Animals, Humans, Hyperplasia, Hypertrophy, Obesity, Syndrome, Adipocytes, Bardet-Biedl Syndrome
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
