Interleukin (IL)-6 mRNA Expression is Stimulated by Insulin, Isoproterenol, Tumour Necrosis Factor Alpha, Growth Hormone, and IL-6 in 3T3-L1 Adipocytes
Abstract
Interleukin (IL)-6 has recently been shown to be an adipocyte-expressed cytokine. Its serum concentrations are elevated in insulin resistance and obesity. For further evaluation of IL-6 gene expression regulation, fully differentiated 3T3-L1 adipocytes were treated with various hormones known to induce insulin resistance. IL-6 mRNA content was measured by quantitative real-time reverse transcription-polymerase chain reaction. Interestingly, treatment of adipocytes with 100 nM insulin, 10 micro M isoproterenol, 10 ng/ml tumour necrosis factor alpha (TNFalpha), and 500 ng/ml growth hormone (GH) for 16 h stimulated IL-6 mRNA expression 2.3-fold, 47-fold, 74-fold, and 1.4-fold, respectively (p < 0.01). In contrast, treatment with 100 nM dexamethasone significantly decreased IL-6 expression to 32 % of control levels (p < 0.01), whereas triiodothyronine and angiotensin 2 did not have any effect. Furthermore, stimulation of IL-6 expression was time-dependent with maximal stimulatory effects detectable after 1 h of insulin, isoproterenol, and GH addition and 12 h of TNFalpha, respectively. Moreover, isoproterenol's effect could be almost completely reversed by pretreatment of 3T3-L1 cells with the beta-adrenergic antagonist propranolol and mimicked by stimulation of G S -proteins with cholera toxin and adenylyl cyclase with forskolin and dibutyryl cAMP, respectively. Finally, IL-6 strongly induced its own expression in a time-dependent fashion. Taken together, our results demonstrate that IL-6 expression in adipocytes is governed by an autocrine positive feedback loop and upregulated by insulin, isoproterenol, TNFalpha, and GH. In concert with this adipocytokine's upregulation in states of decreased insulin sensitivity such as obesity and diabetes, the data support a possible role of IL-6 as a selectively regulated mediator of insulin resistance.
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In vitro studies demonstrate that IL-6 can induce insulin resistance in isolated 3T3-L1 adipocytes and in mice.
“In vitro studies demonstrate that IL-6 can induce insulin resistance in isolated 3T3-L1 adipocytes [51, 52] and in mice [53].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [52]
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- Authors
- Fasshauer, M., Klein, J., Lossner, U., & Paschke, R.
- Affiliations
- Leipzig University (DE)
- University of Lübeck (DE)
- Venue
- Hormone and Metabolic Research
- Publisher
- Georg Thieme Verlag KG
- Published
- 2003-03
- Volume
- 35
- Issue
- 3
- Pages
- 147-152
- ISSN
- 0018-5043 (ISSN-L)
- 1439-4286
- OpenAlex
- W2055531679
- Cited by
- 151
- References
- 0
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 9 · 2022: 1 · 2021: 3 · 2020: 6 · 2019: 6 · 2018: 2 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 3 · 2013: 7 · 2012: 10
- FWCI
- 9.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hormone and Metabolic Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- interleukin-6, adipocytes, 3T3-L1 cells, insulin resistance, gene expression regulation, isoproterenol, beta-adrenergic signaling, propranolol, TNF-α, growth hormone, dexamethasone, obesity, diabetes mellitus, adipokines
- MeSH terms
- Adenylyl Cyclases, Adrenergic beta-Agonists, Animals, Cholera Toxin, Bucladesine, Enzyme Activation, Colforsin, Insulin, Insulin Resistance, Isoproterenol, Kinetics, Receptors, Adrenergic, beta, RNA, Messenger, Growth Hormone, Tumor Necrosis Factor-alpha, Interleukin-6, Gene Expression, Adipocytes, GTP-Binding Protein alpha Subunits, Gs, 3T3-L1 Cells, Mice
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