What question did this study set out to answer?

To investigate whether and how the proinflammatory cytokine interleukin-1β alters insulin signaling and glucose transport in fat cells.

October 13, 2006EndocrinologyOpen Access

Interleukin-1β-Induced Insulin Resistance in Adipocytes through Down-Regulation of Insulin Receptor Substrate-1 Expression

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Authors

JJJennifer JagerInserm TGThierry GrémeauxCentre Méditerranéen de Médecine Moléculaire MCMireille CormontInserm

Discussion

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Implication

In vitro study demonstrates interleukin-1β impairs insulin signaling in adipocytes by down-regulating IRS-1, highlighting a direct cytokine-driven mechanism in insulin resistance.

Key Points

To investigate whether and how the proinflammatory cytokine interleukin-1β alters insulin signaling and glucose transport in fat cells.
Treated murine 3T3-L1 and human adipocytes with acute and prolonged regimens of interleukin-1β.
Evaluated glucose uptake, Glut 1 and Glut 4 transporter translocation, and insulin signaling cascades including IRS-1, protein kinase B, and AS160 phosphorylation.
Applied pharmacological ERK inhibitors to determine the signaling pathway driving interleukin-1β-mediated IRS-1 down-regulation.
Chronic IL-1β exposure reduced insulin-stimulated glucose uptake and impaired Glut 4 plasma membrane translocation without affecting acute insulin responses.
IL-1β selectively diminished IRS-1 expression, tyrosine phosphorylation, downstream protein kinase B activation, and AS160 phosphorylation in both 3T3-L1 and human adipocytes, leaving IRS-2 unaffected.
Pharmacological inhibition of ERK completely prevented IL-1β-induced repression of IRS-1 mRNA and partially restored IRS-1 protein levels, protein kinase B activation, and Glut 4 translocation.

Cite This Study

Jager et al. (2006) studied this question.

synapsesocial.com/papers/69ff8dde831589f3542d9741 https://doi.org/10.1210/en.2006-0692

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October 13, 2006EndocrinologyOpen Access

Interleukin-1β-Induced Insulin Resistance in Adipocytes through Down-Regulation of Insulin Receptor Substrate-1 Expression

View Full Paper

Ask AI

Bookmark

Authors

JJJennifer JagerInserm TGThierry GrémeauxCentre Méditerranéen de Médecine Moléculaire MCMireille CormontInserm

Discussion

Member takes

Implication

In vitro study demonstrates interleukin-1β impairs insulin signaling in adipocytes by down-regulating IRS-1, highlighting a direct cytokine-driven mechanism in insulin resistance.

Key Points

To investigate whether and how the proinflammatory cytokine interleukin-1β alters insulin signaling and glucose transport in fat cells.
Treated murine 3T3-L1 and human adipocytes with acute and prolonged regimens of interleukin-1β.
Evaluated glucose uptake, Glut 1 and Glut 4 transporter translocation, and insulin signaling cascades including IRS-1, protein kinase B, and AS160 phosphorylation.
Applied pharmacological ERK inhibitors to determine the signaling pathway driving interleukin-1β-mediated IRS-1 down-regulation.
Chronic IL-1β exposure reduced insulin-stimulated glucose uptake and impaired Glut 4 plasma membrane translocation without affecting acute insulin responses.
IL-1β selectively diminished IRS-1 expression, tyrosine phosphorylation, downstream protein kinase B activation, and AS160 phosphorylation in both 3T3-L1 and human adipocytes, leaving IRS-2 unaffected.
Pharmacological inhibition of ERK completely prevented IL-1β-induced repression of IRS-1 mRNA and partially restored IRS-1 protein levels, protein kinase B activation, and Glut 4 translocation.

Cite This Study

Jager et al. (2006) studied this question.

synapsesocial.com/papers/69ff8dde831589f3542d9741 https://doi.org/10.1210/en.2006-0692

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