Obesity Activates a Program of Lysosomal-Dependent Lipid Metabolism in Adipose Tissue Macrophages Independently of Classic Activation
Open accessAbstract
Obesity activates a complex systemic immune response that includes the recruitment of macrophages and other immune cells to key metabolic tissues. Current models postulate that obesity and excess lipids classically activate macrophages, polarizing them toward an M1 (inflammatory) state. Little is known about noninflammatory functions of adipose tissue macrophages (ATMs). Here, we show that the expansion of adipose tissue (AT) across models of obesity induces a program of lysosome biogenesis in ATMs and is associated with lipid catabolism but not a classic inflammatory phenotype. This program is induced by factors produced by AT and is tightly coupled to lipid accumulation by ATMs. Inhibition of ATM lysosome function impairs lipid metabolism and increases lipid content in ATMs and reduces whole AT lipolysis. These data argue that ATMs contribute quantitatively to the development of obesity-induced inflammation but also serve an important role in lipid trafficking independent of their inflammatory phenotype.
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Among obese individuals, macrophage phenotype can change, indicating dominance of proinflammatory M1-polarized macrophages over M2 macrophages involved in anti-inflammatory and reparative mechanisms.
“Among obese individuals, it is possible for the phenotype of macrophages to change, indicating the dominance of proinflammatory M1-polarized macrophages over M2 macrophages involved in anti-inflammatory and reparative mechanisms.”
From New Developments in Pharmacological Treatment of Obesity and Type 2 Diabetes—Beyond and within GLP-1 Receptor Agonists (2024) · cites this paper as [13]
The Discussion says the authors did not observe an obesity-driven switch from M2 to M1 macrophages. The Results likewise conclude that obesity does not induce a simple M1-polarized switch in adipose tissue macrophages. These findings are primarily from obese mice, so they do not establish the claimed M1 dominance among obese individuals. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe molecular profile of foamy microglia may reflect metabolic reprogramming associated with the chronic nature of the lesion.
“which may potentially reflect metabolic reprogramming associated with the chronic nature of the lesion14,18,50.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [50]
The Results section (“Obesity Activate Lysosome Biogenesis in ATMs”; page unavailable) reports an obesity-associated transcriptional program of lysosome biogenesis in adipose tissue macrophages. Another Results section (“Adipose Tissue Induces Lysosome Biogenesis, but Not Inflammatory Polarization, of Macrophages”; page unavailable) links lipid accumulation to changes in lipid-handling and lysosomal genes. This supports the possibility of metabolic reprogramming in lipid-laden macrophages, but the paper does not study foamy microglia or chronic lesions. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLack of classical pro-inflammatory signaling has been previously found in MS lesions by mass cytometry of microglia and matches the lipid-induced lysosomal phenotype described in other diseases.
“This lack of classical pro-inflammatory signaling has been previously found in MS lesions by mass cytometry of microglia49 and matches the lipid-induced lysosomal phenotype described in other diseases14,18,50,51.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [50]
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- Authors
- Xu, X., Grijalva, A., Skowronski, A., van Eijk, M., Serlie, M. J., & Ferrante, A. W.
- Affiliations
- Columbia University Irving Medical Center (US)
- Amsterdam UMC Location University of Amsterdam (NL)
- Corresponding author
- Ferrante, Anthony W.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 18
- Issue
- 6
- Pages
- 816-830
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3939841
- OpenAlex
- W1991309264
- Cited by
- 523
- References
- 8
- Citations by year
- 2026: 23 · 2025: 34 · 2024: 44 · 2023: 32 · 2022: 38 · 2021: 61 · 2020: 63 · 2019: 51 · 2018: 47 · 2017: 44 · 2016: 37 · 2015: 22 · 2014: 24 · 2013: 1
- FWCI
- 20.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK007647, DK-063608, R56DK066525, DK026687, (DK066525, P30DK026687, P30DK063608, T32DK007647, R01DK066525)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- obesity, adipose tissue macrophages, lysosomal biogenesis, lipid metabolism, lipid degradation, lipid accumulation, macrophage polarization, M1 macrophages, adipose tissue lipolysis, lipid trafficking, obesity-associated inflammation
- MeSH terms
- Adipose Tissue, Animals, Insulin Resistance, Lipolysis, Lysosomes, Macrophages, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Obesity, Phenotype, Leptin, Lipid Metabolism, Mice
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