The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Interleukin-1β-Induced Insulin Resistance in Adipocytes through Down-Regulation of Insulin Receptor Substrate-1 Expression
Open accessAbstract
Inflammation is associated with obesity and insulin resistance. Proinflammatory cytokines produced by adipose tissue in obesity could alter insulin signaling and action. Recent studies have shown a relationship between IL-1β level and metabolic syndrome or type 2 diabetes. However, the ability of IL-1β to alter insulin signaling and action remains to be explored. We demonstrated that IL-1β slightly increased Glut 1 translocation and basal glucose uptake in 3T3-L1 adipocytes. Importantly, we found that prolonged IL-1β treatment reduced the insulin-induced glucose uptake, whereas an acute treatment had no effect. Chronic treatment with IL-1β slightly decreased the expression of Glut 4 and markedly inhibited its translocation to the plasma membrane in response to insulin. This inhibitory effect was due to a decrease in the amount of insulin receptor substrate (IRS)-1 but not IRS-2 expression in both 3T3-L1 and human adipocytes. The decrease in IRS-1 amount resulted in a reduction in its tyrosine phosphorylation and the alteration of insulin-induced protein kinase B activation and AS160 phosphorylation. Pharmacological inhibition of ERK totally inhibited IL-1β-induced down-regulation of IRS-1 mRNA. Moreover, IRS-1 protein expression and insulin-induced protein kinase B activation, AS160 phosphorylation, and Glut 4 translocation were partially recovered after treatment with the ERK inhibitor. These results demonstrate that IL-1β reduces IRS-1 expression at a transcriptional level through a mechanism that is ERK dependent and at a posttranscriptional level independently of ERK activation. By targeting IRS-1, IL-1β is capable of impairing insulin signaling and action, and could thus participate in concert with other cytokines, in the development of insulin resistance in adipocytes.
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Cites
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Cited by
Mechanisms of Insulin Action and Insulin Resistance
Petersen, M. C., & Shulman, G. I. (2018) · Physiological Reviews · doi:10.1152/physrev.00063.2017 · Cited by 3,028
The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
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Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling
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Metadata
- Authors
- Jager, J., Grémeaux, T., Cormont, M., Le Marchand-Brustel, Y., & Tanti, J.-F.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2007-01-01
- Volume
- 148
- Issue
- 1
- Pages
- 241-251
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2112620654
- Cited by
- 695
- References
- 13
- FWCI
- 14.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Jager, J., Grémeaux, T., Cormont, M., Le Marchand-Brustel, Y., & Tanti, J.-F. (2007). Interleukin-1β-Induced Insulin Resistance in Adipocytes through Down-Regulation of Insulin Receptor Substrate-1 Expression. Endocrinology. https://doi.org/10.1210/en.2006-0692
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