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Showing posts with the label Tumor Necrosis Factor (TNF-α) NEFA/FFA

Adipose Tissue & Adipokines

Normally these days I'd put this in the library, since I'm not really going to blog on this, but I thought this paper a good one to share. Adipose tissue and adipokines: for better or worse In recent years, it has been recognized that adipose tissue (WAT) secretes a number of bioactive peptides and proteins, collectively termed “adipokines”.  These WAT-derived factors play a central role in whole body homeostasis by influencing a variety of biological and physiological processes, including food intake, regulation of energy balance, insulin action, lipid and glucose metabolism, angiogenesis and vascular remodeling, regulation of blood pressure and coagulation. The present review is focused on a restricted number of adipokines, which have been implicated in vascular (angiotensinogen, PAI-1) and energy and glucose homeostasis (ASP, TNFα, IL-6, resistin, leptin, adiponectin).  

Free Fatty Acids and Cytokines Induce Pancreatic ß-Cell Apoptosis by Different Mechanisms

Free Fatty Acids and Cytokines Induce Pancreatic ß-Cell Apoptosis by Different Mechanisms (I've scrubbed the distracting reference numbers from some excerpts of the introduction and I'm also going to try to cite only the information pertinent to T2) Hypercaloric diets containing large amounts of fat, also called the Western diet, contribute to a major extent to the increasing prevalence of obesity and type 2 diabetes mellitus (T2DM). T2DM is characterized by peripheral insulin resistance, pancreatic ß-cell dysfunction, and decreased ß-cell mass associated with increased rates of ß-cell apoptosis. Elevated levels of circulating free fatty acids (FFAs) contribute to the pathogenesis of T2DM. High concentrations of FFAs lead to both impairment of insulin action and ß-cell dysfunction.  Moreover, FFAs have been shown to cause ß -cell death, mainly by apoptosis.  Of note, increased adiposity is associated not only with increa...

Comparative Fatty Acid Toxicity on Macrophages

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Comparative toxicity of fatty acids on a macrophage cell line (J774) In the present study, the cytotoxicity of palmitic, stearic, oleic, linoleic, arachidonic, docosahexaenoic and eicosapentaenoic acids on a macrophage cell line (J774) was investigated. The induction of toxicity was investigated by changes in cell size, granularity, membrane integrity, DNA fragmentation and phosphatidylserine externalization by using flow cytometry. Fluorescence microscopy was used to determine the type of cell death (Acridine Orange/ethidium bromide assay). The possible mechanisms involved were examined by measuring mitochondrial depolarization, lipid accumulation and PPARγ (peroxisome-proliferator-activated receptor γ ) activation. The results demonstrate that fatty acids induce apoptosis and necrosis of J774 cells. At high concentrations, fatty acids cause macrophage death mainly by necrosis. The cytotoxicity of the fatty acids was not strictly related ...

Aspirin for Insulin Resistance?

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I have just recently come across what seems to be a treasure trove of research indicating salicylates (e.g. acetylsalicylic acid aka aspirin) .  Much of the research is in rodents, but the glycemic lowering properties of this common drug are well known (apparently) and documented in humans, but seemingly ignored?   Here's one:   Reversal of Obesity- and Diet-Induced Insulin Resistance with Salicylates or Targeted Disruption of Ikkß   (Full text is available with FREE registration for anyone interested.  You fill out name and they ask for phone/fax info but I left that blank and had no issues.) We show that high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing   insulin signaling. Activation or overexpression of the I B kinase    (IKK ) attenuated insulin signaling in cultured cells, whereas   IKK  inhibition reversed insulin resistance. Thus, IKK , rather   th...

Aspirin for Insulin Resistance?

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I have just recently come across what seems to be a treasure trove of research indicating salicylates (e.g. acetylsalicylic acid aka aspirin) improve insulin sensitivity and lower blood glucose levels.  Much of the research is in rodents, but the glycemic lowering properties of this common drug are well known (apparently) and documented in humans, but seemingly ignored?   Here's one:   Reversal of Obesity- and Diet-Induced Insulin Resistance with Salicylates or Targeted Disruption of Ikkß   (Full text is available with FREE registration for anyone interested.  You fill out name and they ask for phone/fax info but I left that blank and had no issues.) We show that high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing   insulin signaling. Activation or overexpression of the I B kinase    (IKK ) attenuated insulin signaling in cultured cells, whereas   IKK  inhibition reve...