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Control of adipose tissue inflammation through TRB1
Anke Ostertag1, Allan Jones, Adam J Rose
11Emmy Noether and Marie Curie Research Group, Molecular Metabolic Control, DKFZ-ZMBH Alliance, German Cancer Research Center Heidelberg, Heidelberg, Germany.
Diabetes
|June 5, 2010
Summary
Tribbles homolog 1 (TRB1) promotes inflammation in white adipose tissue (WAT) and exacerbates obesity. TRB1 deficiency protects against diet-induced obesity by reducing inflammatory cytokine production in adipocytes.
Area of Science:
- Metabolic disease research
- Adipose tissue biology
- Inflammation and immunity
Background:
- White adipose tissue (WAT) is crucial for energy homeostasis but its dysfunction contributes to obesity and type 2 diabetes.
- Inflammatory responses in adipocytes are implicated in WAT dysfunction and metabolic diseases.
- The pseudokinase Tribbles (TRB) 3 regulates glucose and lipid homeostasis, suggesting broader roles for the TRB gene family.
Purpose of the Study:
- To investigate the role of the TRB gene family in integrating metabolic and inflammatory pathways.
- To determine the function of TRB family members in white adipose tissue (WAT).
Main Methods:
- Profiled expression patterns of TRB1 and TRB13 in WAT under healthy and stressed conditions.
- Functionally characterized TRB1 using loss-of-function animal models and primary adipocytes.
Main Results:
- TRB1 expression is upregulated during acute and chronic inflammation in WAT.
- TRB1 deficiency impairs cytokine gene expression in white adipocytes.
- TRB1 acts as a nuclear coactivator for RelA, promoting proinflammatory cytokine induction in adipocytes.
- TRB1 deficiency protects against high-fat diet-induced obesity.
Conclusions:
- TRB1 plays a dual role as a target and activator of inflammatory signaling in WAT.
- TRB1 may amplify proinflammatory responses in conditions like sepsis, insulin resistance, and type 2 diabetes.
- Targeting TRB1 could offer therapeutic strategies for metabolic and inflammatory diseases.
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