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Weight loss and lipolysis promote a dynamic immune response in murine adipose tissue
Open accessAbstract
Obesity elicits an immune response characterized by myeloid cell recruitment to key metabolic organs, including adipose tissue. However, the response of immune cells to nonpathologic metabolic stimuli has been less well studied, and the factors that regulate the metabolic-dependent accumulation of immune cells are incompletely understood. Here we characterized the response of adipose tissue macrophages (ATMs) to weight loss and fasting in mice and identified a role for lipolysis in ATM recruitment and accumulation. We found that the immune response to weight loss was dynamic; caloric restriction of high-fat diet-fed mice led to an initial increase in ATM recruitment, whereas ATM content decreased following an extended period of weight loss. The peak in ATM number coincided with the peak in the circulating concentrations of FFA and adipose tissue lipolysis, suggesting that lipolysis drives ATM accumulation. Indeed, fasting or pharmacologically induced lipolysis rapidly increased ATM accumulation, adipose tissue chemoattractant activity, and lipid uptake by ATMs. Conversely, dietary and genetic manipulations that reduced lipolysis decreased ATM accumulation. Depletion of macrophages in adipose tissue cultures increased expression of adipose triglyceride lipase and genes regulated by FFA, and increased lipolysis. These data suggest that local lipid fluxes are central regulators of ATM recruitment and that once recruited, ATMs form lipid-laden macrophages that can buffer local increases in lipid concentration.
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“This was indeed observed by Kosteli et al. during chronic weight loss, during which they report that a progressive decrease in lipolysis and ATMΦ content followed 21 days of caloric restriction (39);”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [39]
Experimental — accuracy not yet measuredIn the citing paper
“Recently, Kosteli and colleagues demonstrated that acute weight loss is unexpectedly associated with a rapid -albeit transient -lipolytic-driven recruitment of macrophages into AT (39), thereby confirming similar reports by Granneman and colleagues (44).”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [39]
In the citing paper
“Ironically, acute weight loss (days 0-7), a 24-hour fast, or pharmacological induction of adipocyte lipolysis using a β3-adrenergic agonist all resulted in a transient accumulation of lipid-laden ATMΦs (an increase of up to 65% of macrophage infiltration was observed).”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [39]
In the citing paper
“We thus challenged animals with ADRB agonists and found that the ADRB3 agonist CL316,243, but not the ADRB1/2 agonist isoproterenol, was sufficient to induce IL6 (Figure 3E and F), consistent with previous reports (Kosteli et al., 2010; Zhang et al., 2014).”
From Origin and function of stress-induced IL-6 in murine models (2020) · cites this paper as Kosteli et al., 2010
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Metadata
- Authors
- Kosteli, A., Sugaru, E., Haemmerle, G., Martin, J. F., Lei, J., Zechner, R., & Ferrante, A. W.
- Affiliations
- Columbia University Irving Medical Center (US)
- University of Graz (AT)
- Corresponding author
- Ferrante, Anthony W.
- Venue
- Journal of Clinical Investigation
- Published
- 2010-10-01
- Volume
- 120
- Issue
- 10
- Pages
- 3466-3479
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2947229
- OpenAlex
- W2129973062
- Cited by
- 726
- References
- 54
- Citations by year
- 2026: 19 · 2025: 38 · 2024: 36 · 2023: 33 · 2022: 31 · 2021: 47 · 2020: 51 · 2019: 45 · 2018: 47 · 2017: 51 · 2016: 48 · 2015: 53 · 2014: 48 · 2013: 63 · 2012: 62
- FWCI
- 41.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Russell Berrie Foundation
- National Institutes of Health (DK026687, DK066525)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-063608, R56DK066525, DK026687, (DK066525, P30DK026687, P30DK063608, R01DK066525)
- 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 macrophages, lipolysis, weight loss, fasting, caloric restriction, obesity, fatty acid uptake, adipose triglyceride lipase, myeloid cell recruitment, lipid metabolism, high-fat diet, macrophage lipid accumulation, chemoattraction
- MeSH terms
- Acyltransferases, Adipose Tissue, Animals, Carboxylic Ester Hydrolases, Cell Movement, Fatty Acids, Nonesterified, Lipase, Lipolysis, Macrophages, Male, Mice, Inbred C57BL, Weight Loss, Mice
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