Characterization of Distinct Subpopulations of Hepatic Macrophages in HFD/Obese Mice
Open accessAbstract
The current dogma is that obesity-associated hepatic inflammation is due to increased Kupffer cell (KC) activation. However, recruited hepatic macrophages (RHMs) were recently shown to represent a sizable liver macrophage population in the context of obesity. Therefore, we assessed whether KCs and RHMs, or both, represent the major liver inflammatory cell type in obesity. We used a combination of in vivo macrophage tracking methodologies and adoptive transfer techniques in which KCs and RHMs are differentially labeled with fluorescent markers. With these approaches, the inflammatory phenotype of these distinct macrophage populations was determined under lean and obese conditions. In vivo macrophage tracking revealed an approximately sixfold higher number of RHMs in obese mice than in lean mice, whereas the number of KCs was comparable. In addition, RHMs comprised smaller size and immature, monocyte-derived cells compared with KCs. Furthermore, RHMs from obese mice were more inflamed and expressed higher levels of tumor necrosis factor-α and interleukin-6 than RHMs from lean mice. A comparison of the MCP-1/C-C chemokine receptor type 2 (CCR2) chemokine system between the two cell types showed that the ligand (MCP-1) is more highly expressed in KCs than in RHMs, whereas CCR2 expression is approximately fivefold greater in RHMs. We conclude that KCs can participate in obesity-induced inflammation by causing the recruitment of RHMs, which are distinct from KCs and are not precursors to KCs. These RHMs then enhance the severity of obesity-induced inflammation and hepatic insulin resistance.
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A brain-liver axis may link chronic stress to hyperglycemia via hepatic inflammation.
“Since pro-inflammatory polarization of immune cells in the liver directly leads to insulin resistance138, a brain–liver axis may link chronic stress to hyperglycemia via hepatic inflammation.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [138]
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- Authors
- Morinaga, H., Mayoral, R., Heinrichsdorff, J., Osborn, O., Franck, N., Hah, N., Walenta, E., Bandyopadhyay, G., Pessentheiner, A. R., Chi, T. J., Chung, H., Bogner-Strauss, J. G., Evans, R. M., Olefsky, J. M., & Oh, D. Y.
- Affiliations
- University of California San Diego (US)
- Instituto de Salud Carlos III (ES)
- Salk Institute for Biological Studies (US)
- Institute of Biochemistry, Graz University of Technology, Graz, Austria
- Corresponding author
- Olefsky, Jerrold M.
- Oh, Da Young
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2014-10-14
- Volume
- 64
- Issue
- 4
- Pages
- 1120-1130
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC4375077
- OpenAlex
- W2171752155
- Cited by
- 175
- References
- 61
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 8 · 2023: 18 · 2022: 22 · 2021: 25 · 2020: 15 · 2019: 15 · 2018: 14 · 2017: 16 · 2016: 16 · 2015: 6 · 2013: 1
- FWCI
- 9.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (DK033651, DK063491, DK074868, DK09062, P30 DK063491, P30 NS047101)
- Austrian Science Fund (DK-MCD W1226, P24143)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- hepatic macrophages, Kupffer cells, obesity, liver inflammation, high-fat diet, macrophage tracking, adoptive transfer, MCP-1, CCR2, TNF-α, interleukin-6, hepatic insulin resistance, monocyte-derived macrophages
- MeSH terms
- Animals, Fatty Liver, Gluconeogenesis, Kupffer Cells, Liver, Macrophages, Male, Mice, Obese, Obesity, Tumor Necrosis Factor-alpha, Interleukin-6, Mice, Receptors, CCR2, Diet, High-Fat
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