The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects
Open accessAbstract
Omega-3 fatty acids (omega-3 FAs), DHA and EPA, exert anti-inflammatory effects, but the mechanisms are poorly understood. Here, we show that the G protein-coupled receptor 120 (GPR120) functions as an omega-3 FA receptor/sensor. Stimulation of GPR120 with omega-3 FAs or a chemical agonist causes broad anti-inflammatory effects in monocytic RAW 264.7 cells and in primary intraperitoneal macrophages. All of these effects are abrogated by GPR120 knockdown. Since chronic macrophage-mediated tissue inflammation is a key mechanism for insulin resistance in obesity, we fed obese WT and GPR120 knockout mice a high-fat diet with or without omega-3 FA supplementation. The omega-3 FA treatment inhibited inflammation and enhanced systemic insulin sensitivity in WT mice, but was without effect in GPR120 knockout mice. In conclusion, GPR120 is a functional omega-3 FA receptor/sensor and mediates potent insulin sensitizing and antidiabetic effects in vivo by repressing macrophage-induced tissue inflammation.
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“The anti-inflammatory effects of omega-3 fatty acids seems to be mediated by binding to the G-protein–coupled receptor 120 and inhibition of NLRP3 inflammasome activity (53,54).”
From Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms (2018) · cites this paper as [53]
In the citing paper
“in macrophages and adipocytes the G-protein coupled receptor GPR120 is an omega-3 sensitive receptor that exhibits anti-inflammatory properties through the suppression of TNF-activation [141]”
From Omega-3 Fatty Acids and Skeletal Muscle Health (2015) · cites this paper as [141]
In the citing paper
“GPR120 expression is negligible in skeletal muscle and would therefore not explain the changes induced by omega-3 PUFAs in tissue culture models [141]”
From Omega-3 Fatty Acids and Skeletal Muscle Health (2015) · cites this paper as [141]
In the citing paper
“In summary, the n-3 PUFAs EPA and DHA can reduce inflammation via their incorporation into membrane phospholipids, where they inhibit the production of pro-inflammatory eicosanoids, reducing of activation of immune cells and the associated release of pro-inflammatory cytokines [71,97,98].”
From Potential Roles of n-3 PUFAs during Skeletal Muscle Growth and Regeneration (2018) · cites this paper as [98]
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Citations
Cites
A SIMPLE METHOD FOR THE ISOLATION AND PURIFICATION OF TOTAL LIPIDES FROM ANIMAL TISSUES
Folch, J., Lees, M., & Stanley, G. H. S. (1957) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)64849-5 · Cited by 65,189
Obesity is associated with macrophage accumulation in adipose tissue
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“Consistent with previous studies (Weisberg et al., 2003; Xu et al., 2003; Nguyen et al., 2007), HFD induced a large increase in F4/80 positive ATMs, which form crown-like structures (CLS) around adipocytes in both WT and GPR120 KO mice.”
InfluentialXu, H., Barnes, G. T., Yang, Q., Tan, G., Yang, D., Chou, C. J., Sole, J., Nichols, A., Ross, J. S., Tartaglia, L. A., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319451 · Cited by 6,760
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“Since chronic tissue inflammation is an important mechanism causing insulin resistance (Xu et al., 2003; Shoelson et al., 2007; Schenk et al., 2008), the anti-inflammatory actions of u-3 FAs exert potent insulin sensitizing effects.”
InfluentialFree fatty acids regulate gut incretin glucagon-like peptide-1 secretion through GPR120
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“Long-chain FAs can activate GPR40 (Itoh et al., 2003) and GPR120 (Hirasawa et al., 2005).”
InfluentialFree fatty acids regulate insulin secretion from pancreatic β cells through GPR40
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“Recently, several groups reported that five orphan receptors, GPR40, GPR41, GPR43, GPR84, and GPR120, can be activated by free fatty acids (FFAs).”
Influentialβ-Arrestin-Dependent Formation of β 2 Adrenergic Receptor-Src Protein Kinase Complexes
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“Interestingly, only the full-length b-arrestin2 coprecipitated with GPR120 and TAB1, while a series of deletion/truncation b-arrestin2 mutants did not, indicating that the interactions are dependent on the complete tertiary structure of b-arrestin2 (Figure S2D; Luttrell et al., 1999).”
Uncovering Molecular Mechanisms Involved in Activation of G Protein-Coupled Receptors
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“…to GPCRs to stimulate and induce a variety of cellular responses via several second messenger pathways; e.g., modulation of cAMP production, the phospholipase C pathway, ion channels, and mitogen-activated protein kinases (Ulloa-Aguirre et al., 1999; Gether, 2000; Schulte and Fredholm, 2003.”
Insulin sensitivity: Modulation by nutrients and inflammation
Schenk, S., Saberi, M., & Olefsky, J. M. (2008) · Journal of Clinical Investigation · doi:10.1172/jci34260 · Cited by 1,191 · cited 5×
“Since chronic macrophage-mediated tissue inflammation is a key mechanism for insulin resistance in obesity, we fed obese WT and GPR120 knockout mice a high-fat diet with or without u-3 FA supplementation.”
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International Journal of Molecular Sciences
Soni, N., Ross, A., Nookaew, I., Scheers, N., Gabrielsson, B., & Sandberg, A.-S. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms · Cited by 10,136
Inflammatory Mechanisms in Obesity
Gregor, M. F., & Hotamisligil, G. S. (2011) · Annual Review of Immunology · doi:10.1146/annurev-immunol-031210-101322 · Cited by 3,754
Human nutrition, the gut microbiome and the immune system
Kau, A. L., Ahern, P. P., Griffin, N. W., Goodman, A. L., & Gordon, J. I. (2011) · Nature · doi:10.1038/nature10213 · Cited by 2,588
Inflammatory links between obesity and metabolic disease
Lumeng, C. N., & Saltiel, A. R. (2011) · Journal of Clinical Investigation · doi:10.1172/jci57132 · Cited by 2,319
Inflammation in obesity, diabetes, and related disorders
Rohm, T. V., Meier, D. T., Olefsky, J. M., & Donath, M. Y. (2022) · Immunity · doi:10.1016/j.immuni.2021.12.013 · Cited by 2,066
Self-citation
Metadata
- Authors
- Oh, D. Y., Talukdar, S., Bae, E. J., Imamura, T., Morinaga, H., Fan, W., Li, P., Lu, W. J., Watkins, S. M., & Olefsky, J. M.
- Affiliations
- University of California San Diego (US)
- Shiga University of Medical Science (JP)
- Corresponding author
- Olefsky, Jerrold M.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2010-09
- Volume
- 142
- Issue
- 5
- Pages
- 687-698
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2956412
- OpenAlex
- W2131094572
- Cited by
- 2,428
- References
- 49
- Citations by year
- 2026: 97 · 2025: 134 · 2024: 123 · 2023: 129 · 2022: 134 · 2021: 180 · 2020: 172 · 2019: 157 · 2018: 158 · 2017: 181 · 2016: 197 · 2015: 177 · 2014: 165 · 2013: 162 · 2012: 143
- FWCI
- 127.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (NIDDK DK033651, DK 074868, DK063491, U54 HD 012303-25)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- GPR120, docosahexaenoic acid, eicosapentaenoic acid, anti-inflammatory activity, insulin sensitivity, insulin resistance, macrophage inflammation, obesity, high-fat diet, G protein-coupled receptors, RAW 264.7 macrophages
- MeSH terms
- Animals, Anti-Inflammatory Agents, Cell Line, Dietary Fats, Humans, Hypoglycemic Agents, Insulin Resistance, Macrophages, Obesity, Fatty Acids, Omega-3, Mice, Knockout, Dietary Supplements, 3T3-L1 Cells, Receptors, G-Protein-Coupled, Mice
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