Adipogenesis and metabolic health
Abstract
Obesity is characterized by increased adipose tissue mass and has been associated with a strong predisposition towards metabolic diseases and cancer. Thus, it constitutes a public health issue of major proportion. The expansion of adipose depots can be driven either by the increase in adipocyte size (hypertrophy) or by the formation of new adipocytes from precursor differentiation in the process of adipogenesis (hyperplasia). Notably, adipocyte expansion through adipogenesis can offset the negative metabolic effects of obesity, and the mechanisms and regulators of this adaptive process are now emerging. Over the past several years, we have learned a considerable amount about how adipocyte fate is determined and how adipogenesis is regulated by signalling and systemic factors. We have also gained appreciation that the adipogenic niche can influence tissue adipogenic capability. Approaches aimed at increasing adipogenesis over adipocyte hypertrophy can now be explored as a means to treat metabolic diseases.
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A key outcome of muscle-adipose crosstalk is the promotion of metabolic flexibility.
“A key outcome of muscle–adipose crosstalk is the promotion of metabolic flexibility”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [89]
The expansion of adipose depots can be driven either by the increase in adipocyte size (hypertrophy), or by the formation of new adipocytes from perivascular preadipocytes and pericytes (hyperplasia).
“The expansion of adipose depots can be driven either by the increase in adipocyte size (hypertrophy), or by the formation of new adipocytes from perivascular preadipocytes and pericytes (hyperplasia).[ 23 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [23]
During transient hyperlipidaemia after food intake, adipose tissues are driven to expand.
“During transient hyperlipidaemia after food intake, adipose tissues are driven to expand.”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [23]
Even before obesity becomes obvious, persistent hyperlipidaemia contributes to fat redistribution, for example, subcutaneous adipose inflammation and lipolysis, fuelling visceral adipose tissue (VAT) expansion.
“Thus, even before obesity becomes obvious, persistent hyperlipidaemia contributes to fat redistribution, for example, subcutaneous adipose inflammation and lipolysis, fuelling visceral adipose tissue (VAT) expansion.[ 23 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [23]
Chronic inflammation in extant adipose depots and other tissues also contribute to the pathophysiology of adipose tissue dysfunction, including the gradual impairment of adipogenesis that contributes to IR and metabolic disease.
“Chronic inflammation in extant adipose depots and other tissues also contribute to the pathophysiology of adipose tissue dysfunction, including the gradual impairment of adipogenesis that contributes to IR and metabolic disease.[ 23 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [23]
After a long period of systemic inflammaging, chronic inflammation in adipose depots leads to systemic atrophy and wasting observed in cachexia and full-blown sarcopenia.
“But after a long period of systemic inflammaging, chronic inflammation in adipose depots would lead to the systemic atrophy and wasting observed in cachexia and full‐blown sarcopenia.[ 23 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [23]
Adipose tissue is capable of expanding to more than double its original size by hypertrophy and/or hyperplasia.
“In fact, AT is remarkably capable of expanding to more than double its original size by hypertrophy (enlargement of the cell size) and/or hyperplasia (increase in cell number) [3].”
From Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance (2024) · cites this paper as [3]
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- Authors
- Ghaben, A. L., & Scherer, P. E.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Scherer, Philipp E.
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2019-01-04
- Volume
- 20
- Issue
- 4
- Pages
- 242-258
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W2908320623
- Semantic Scholar
- 4fcd08092b207de7bf166354cd3000e12504500a
- Cited by
- 1,395
- References
- 248
- Citations by year
- 2026: 128 · 2025: 209 · 2024: 212 · 2023: 218 · 2022: 219 · 2021: 207 · 2020: 140 · 2019: 61
- FWCI
- 18.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- adipogenesis, obesity, metabolic health, adipocyte hypertrophy, adipocyte hyperplasia, adipose tissue expansion, white adipose tissue, metabolic disorders, cancer risk
- MeSH terms
- Animals, Cell Differentiation, Health, Humans, Obesity, Signal Transduction, Adipocytes, Adipogenesis
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