Why do anti-inflammatory therapies fail to improve insulin sensitivity? - Wikidata - wikimedia - TriplyDB

Why do anti-inflammatory therapies fail to improve insulin sensitivity?

Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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In immune defense: redefining the role of the immune system in chronic disease.Harnessing the beneficial properties of adipogenic microbes for improving human health.Novel Agents for the Treatment of Type 2 Diabetes.Quantitative Systems Pharmacology: A Framework for Context.Reassessing lipid metabolism and its potentialities in the prediction of cardiovascular risk.Inflammation Improves Glucose Homeostasis through IKKβ-XBP1s Interaction.Anti-Diabetic Agent Sodium Tungstate Induces the Secretion of Pro- and Anti-Inflammatory Cytokines by Human Kidney Cells.On the analysis of complex biological supply chains: From Process Systems Engineering to Quantitative Systems Pharmacology.

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

http://www.wikidata.org/entity/Q37950733

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Acta Pharmacologica Sinica

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Why do anti-inflammatory therapies fail to improve insulin sensitivity?

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Jian-ping Ye

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Zhan-guo Gao

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Inflammation and insulin resistance

Protein kinase C Theta inhibits insulin signaling by phosphorylating IRS1 at Ser(1101)

S6K directly phosphorylates IRS-1 on Ser-270 to promote insulin resistance in response to TNF-(alpha) signaling through IKK2

The p65 subunit is responsible for the strong transcription activating potential of NF-kappa B

Nuclear receptor corepressors partner with class II histone deacetylases in a Sin3-independent repression pathway

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity

Obesity is associated with macrophage accumulation in adipose tissue

Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307)

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182-188

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scholarly article

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10.1038/APS.2011.131

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2

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33

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2011-10-31T00:00:00Z

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51756219

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22036866

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3270211

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