Regulation of Adipose Cell Number in Man
Abstract
1. Adipose tissue mass is dependent on both the average volume and the number of its constituent adipocytes. Significant alteration in body mass involves alteration in both adipocyte volume and number. 2. Increases in adipocyte number occur via replication and differentiation of preadipocytes, a process which occurs throughout life. Decreases in adipocyte number occur via preadipocyte and adipocyte apoptosis, and possibly adipocyte dedifferentiation. 3. Overall regulation of adipose mass involves endocrine, paracrine and possibly autocrine systems. Hypothalamic centres appear to control appetite, metabolic rate and activity levels in a co-ordinated manner. Within the hypothalamus, known weight regulatory molecules include glucagon-like peptide-1, neuropeptide Y and leptin. Leptin is a major afferent signal from adipose tissue to the hypothalamus, providing information on overall adipose tissue mass. However, the precise means by which the hypothalamus signals to adipose tissue is less well understood. 4. In adipose tissue, known molecular regulators of adipose cell number include insulin, ligands for the peroxisome proliferator activated receptor-γ, retinoids, corticosteroids and tumour necrosis factor-α. The net effect of these and other regulators is to effect a concerted alteration in adipocyte volume and number. This review largely focuses on the control of fat cell acquisition and loss and the influence of these processes on adipose tissue mass and regional distribution.
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Adipose tissue is highly plastic and has the capacity for unlimited growth throughout adulthood.
“Though its development begins prenatally, quite uniquely, it has the capacity for unlimited growth throughout adulthood.”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [18]
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References 37 · Cited by 406
- Authors
- Prins, J. B., & O'rahilly, S.
- Affiliations
- University of Cambridge (GB)
- Departments of Medicine and Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Cambridge, U.K.
- ORCID
- Prins, Johannes B.
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 1997-01-01
- Volume
- 92
- Issue
- 1
- Pages
- 3-11
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- OpenAlex
- W81827842
- Cited by
- 406
- References
- 37
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 9 · 2022: 7 · 2021: 9 · 2020: 3 · 2019: 8 · 2018: 7 · 2017: 12 · 2016: 14 · 2015: 13 · 2014: 25 · 2013: 22 · 2012: 21
- FWCI
- 11.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- adipocyte number, adipose tissue mass, preadipocyte differentiation, adipocyte apoptosis, adipocyte dedifferentiation, hypothalamic regulation of appetite, leptin, glucagon-like peptide-1, neuropeptide Y, insulin, PPARγ, retinoids, corticosteroids, TNF-α, body fat distribution, body weight regulation
- MeSH terms
- Adipose Tissue, Body Composition, Cell Count, Cell Division, Hormones, Humans, Apoptosis, Adipocytes, Cell Size
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