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Nathan Goodyear

Fatty acid-induced mitochondrial uncoupling in ... [Diabetologia. 2007] - PubMed - NCBI - 0 views

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    how increase FFA uncouples mitochondria.  Role in development of insulin resistance and type II diabetes
Nathan Goodyear

Figure 1 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

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    nice diagram of how adipocyte dysfunction leads to inflammation and insulin resistance, and increase FFA.
Nathan Goodyear

Figure 2 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

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    chronic, not acute, inflammation disrupts normal triglyceride metabolism and results in increased FFA
Nathan Goodyear

Figure 3 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

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    TNF-alpha downregulates PPAR and increases FFA
Nathan Goodyear

Figure 5 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

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    proposed TNF-alpha downregulation of PPAR and resultant increase in FFA and thus inflammation, insulin resistance, diabetes...
Nathan Goodyear

Free fatty acids and insulin resistance : Current Opinion in Clinical Nutrition & Metab... - 0 views

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    FFA excess contributes to inflammation, insulin resistance, and obesity
Nathan Goodyear

Innate Immune Pathway Links Obesity to Insulin Resistance - 0 views

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    insulin resistance leads to excess FFA, obesity and activation of the innate immune signaling.  This uses TLR4  and stimulates NF-KappaB transcription.  The result is inflammation and associated inflammatory disease conditions.
Nathan Goodyear

Toll-Like Receptor-4 Mediates Vascular Inflammation and Insulin Resistance in Diet-Indu... - 0 views

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    high saturated fat intake (excess FFA) shown to contribute to obesity through TLR4 receptors.  TLR4 receptors are mediators in the innate immunity.   The result will be both IKK-Beta and NF-KappaB.
Nathan Goodyear

Access : FFA-Induced Adipocyte Inflammation and Insulin Resistance: Involvement of ER S... - 0 views

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    elevated FFA (free-fatty acids) shown to produce inflammation and insulin resistance through endoplasmic reticulum stress.  The main target in this pathway is IKK-Beta overexpression.
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