Deficiency in interleukin-18 promotes differentiation of brown adipose tissue resulting in fat accumulation despite dyslipidemia
Open accessAbstract
The cytokine, interleukin-18 (IL-18), was originally identified as an interferon-γ-inducing proinflammatory factor; however, there is increasing evidence suggesting that it has non-immunological effects on physiological functions. We have previously investigated the potential pathophysiological relationship between IL-18 and dyslipidemia, non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which were mediated by lipid energy imbalance. Therefore, herein we focused on brown adipocytes (BAs) and brown adipose tissue (BAT) related to energy consumption as non-shivering thermogenesis. Il18 −/− male mice were generated on the C57Bl/6 background, and littermate C57Bl/6 Il18 +/+ male mice were used as controls. To reveal the direct effect of IL-18, primary cell cultures derived from both mice were established. Moreover, for molecular analysis, microarray, quantitative reverse transcription PCR and western blotting were performed using 6 and 12 weeks old mice. To evaluate the short- and long-term effects of IL-18 on BAT, recombinant IL-18 was administered for 2 and 12 weeks, respectively. Compared with Il18 +/+ mice, BAT of Il18 −/− mice showed earlier differentiation and lipid accumulation. To examine the direct effect of IL-18 on BAT, BA cell cultures were established. Myogenic factor 5 -expressing adipose precursor cells were extracted from Il18 +/+ and Il18 −/− mice. PR domain containing 16 (PRDM16), a differentiation inducer, was strongly expressed in Il18 −/− BAs, and uncoupling protein 1, a thermogenic and differentiation marker, was upregulated, resulting in the promotion of BA differentiation. Moreover, PRDM16-dependent and independent molecules related to BAT function, such as fibroblast growth factor 21, were activated. These findings were confirmed by comparing Il18 +/+ and Il18 −/− mice at 6 and 12 weeks of age. Additional analyses of the molecular mechanisms influencing the ‘Quantity of adipocytes’ identified three associated genes, apolipoprotein C3 ( Apoc3 ), insulin-induced gene 1 ( Insig1 ) and vitamin D (1,25-dihydroxyvitamin D3) receptor ( Vdr ). Intravenous administration of IL-18 not only significantly improved the expression of some of these genes, but it also significantly decreased the adipocytes’ size. This study demonstrated the critical function of IL-18 in differentiation and lipid metabolism in BAs. Furthermore, IL-18 may contribute to novel treatments by improving the energy imbalance.
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C57BL7 mice deficient for IL-18 exhibit larger brown adipocytes and higher UCP-1 expression in BAT compared to wild-type littermates.
“Indeed, C57BL7 mice deficient for IL-18 are extremely sensitive to obesity but also exhibit larger brown adipocytes and a higher UCP-1 expression in BAT compared to wild-type littermates [240].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [240]
Exogenous administration of IL-18 in IL-18 deficient mice restores adipocyte size and UCP-1 expression.
“To support the role of IL-18 in this process, exogenous administration of IL-18 in these mice restores the adipocyte size as well as the expression of UCP-1 [240].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [240]
C57BL7 mice deficient for IL-18 are extremely sensitive to obesity.
“Indeed, C57BL7 mice deficient for IL-18 are extremely sensitive to obesity but also exhibit larger brown adipocytes and a higher UCP-1 expression in BAT compared to wild-type littermates [240].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [240]
IL-18 seems to regulate UCP-1 expression in adipose tissues.
“In addition to its immune role, IL-18 also seems to regulate UCP-1 expression in adipose tissues.”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [240]
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- Authors
- Yamanishi, K., Maeda, S., Kuwahara-Otani, S., Hashimoto, T., Ikubo, K., Mukai, K., Nakasho, K., Gamachi, N., El-Darawish, Y., Li, W., Okuzaki, D., Watanabe, Y., Yamanishi, H., Okamura, H., & Matsunaga, H.
- Affiliations
- Hyogo Medical University (JP)
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Corresponding author
- Matsunaga, Hisato
- ORCID
- Venue
- Journal of Translational Medicine
- Published
- 2018-11-19
- Volume
- 16
- Issue
- 1
- Pages
- 314-314
- ISSN
- 1479-5876 (ISSN-L)
- PMC
- PMC6245626
- OpenAlex
- W2901070596
- Cited by
- 15
- References
- 56
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 3 · 2019: 2
- FWCI
- 0.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Translational Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- 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 › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- IL-18, brown adipose tissue, brown adipocyte differentiation, dyslipidemia, non-shivering thermogenesis, PRDM16, UCP1, FGF21, apolipoprotein C-III, INSIG1, vitamin D receptor, adipogenesis, lipid accumulation, energy metabolism
- MeSH terms
- Animals, Adipose Tissue, Brown, Cell Differentiation, Fatty Liver, Male, Mice, Inbred C57BL, Recombinant Proteins, Stem Cells, Interleukin-18, Thermogenesis, Adiposity, Adipogenesis, Dyslipidemias, Lipid Metabolism
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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