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Nathan Goodyear

The omega-3 index as a risk factor for coronary heart disease - 0 views

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    Omega-3 fatty acids can be used to predict risk for coronary heart disease death, especially sudden cardiac death.
Nathan Goodyear

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

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

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | ScienceDirect.com - 0 views

  • A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
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  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
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    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

Pathogenesis of non-alcoholic fatty liver disease - 0 views

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    The fastest growing liver disease today is NAFLD, which is a direct result of the rising obesity epidemic.  This is a good review of the current understanding on the pathophysiology of NAFLD.
Nathan Goodyear

Adipose Tissue Inflammation in Obesity and Metabolic Syndrome - - Satoshi Nishimura - Discovery Medicine - 0 views

  • Activation of inflammatory pathways in adipocytes impairs triglyceride storage and increases release of free fatty acids, an excess of which is known to induce insulin resistance in muscle and liver
  • recent studies have shown that large numbers of macrophages infiltrate obese adipose tissue,
  • It has been postulated that a paracrine loop involving free fatty acids and inflammatory cytokines establishes a vicious cycle between adipocytes and macrophages that propagates the inflammation
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  • not only does interrupting the accumulation of macrophages within obese adipose tissue suppresses adipose inflammation in various animal models, it also ameliorates systemic insulin resistance and metabolic abnormalities, suggesting macrophages are key effector cells involved in adipose inflammation
  • activation of the leukocyte adhesion cascade, a hallmark of inflammation
  • Thus, obese visceral adipose tissue is clearly a site of chronic inflammation
  • CD8+ T cells within obese adipose tissue induce activation and migration of monocytes/macrophages, and in cooperation with the adipose tissue, they also induce macrophage differentiation. At the same time, obese adipose tissue activates CD8+ T cells, creating a vicious cycle involving CD8+ T cells, macrophages, and obese adipose tissue that propagates local inflammation
  • In obese adipose tissue there is a shift to dominance of CD8+ and TH1 T cells, which appears to propagate inflammation
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    fascinating read how the immune system and resultant inflammation results in obesity.
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

Effect of omega-3 fatty acids on inten... [Int J Gynaecol Obstet. 2012] - PubMed - NCBI - 0 views

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    Omega-3 reduced the intensity of menstrual cramps.  Omega-3 reduced the need for rescue ibuprofen.
Nathan Goodyear

Adiponectin translation is increased by the PPARγ agonists pioglitazone and ω-3 fatty acids - 0 views

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    Omeg-3, DHA and EPA, increased adiponectin production.  In addition, blockade of the PPAR-gamma resulted in a reduction in adiponectin production.  Thus PPAR gamma activation results in adiponectin production by adipocytes.
Nathan Goodyear

JAMA Network | JAMA: The Journal of the American Medical Association | Association of Dietary Intake of Fat and Fatty Acids With Risk of Breast Cancer - 0 views

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    Nurses' Health study analysis finds no increased breast cancer risk with low fat diet.  This was a meta-analysis of almost 90,000 women.
Nathan Goodyear

n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases - 0 views

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    Omega 3 and inflammation.  Good review of the biochemistry of inflammation and the interaction of omega-3 as a disruptor of inflammation.
Nathan Goodyear

Annals of Internal Medicine | Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis - 0 views

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    Meta-analysis finds no improvement with cardiovascular risk from low saturated fats.  This is not the first study to show this.  The weakness of this is that this study is a meta-analysis.  This needs to be taken in context and applied individually.  The take home is that universal restriction of saturated fats is not the holy grail of nutrition.
Nathan Goodyear

Influence of alpha-lipoic acid on lipid ... [Diabetes Obes Metab. 2004] - PubMed - NCBI - 0 views

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    Numerous deletorious effects are seen in high fructose diets: elevated Triglyceride production, fatty liver, insulin resistance, increased VLDL production and secretion, increased deposit of TG in muscle and increased muscle insulin resistance.  Alpha lipoic Acid is shown to counter these effects in rat model.
Nathan Goodyear

Oxidant stress, ant... [Prostaglandins Leukot Essent Fatty Acids. 1997] - PubMed - NCBI - 0 views

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    low EPA and DHA found in patients with Lupus.  The authors of this article went so far as to say that lipid peroxides, NO, and anti-oxidants should be a part of the work up for patients with Lupus.
Nathan Goodyear

Hypometabolism as a therapeutic target in Alzheimer's disease - 0 views

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    Medium chain fatty acids, such as cocconut oil, benefit brain with glucose hypometabolism problems such as in Alzheimer's disease.
Nathan Goodyear

Plasma fatty acids as predictors of glycaemia and type 2 diabetes. - PubMed - NCBI - 0 views

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    Palmitoleic acid and estimated D6D activity found to positively correlate with diabetes and worsening glucose control;  In contrast, linoleum acid found to be inversely associated with glucose control and Diabetes development.
Nathan Goodyear

Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

  • concussive brain injury is a major cause of neuropsychological disability in spite of no obvious neuronal death
  • TBI elicits oxidative damage to plasma membrane phospholipids
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain, where the DHA-containing phospholipids contribute to plasma membrane biogenesis and receptor signaling
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  • curcumin has potent anti-inflammatory and antioxidant activities that can function to reduce oxidative damage and cognitive deficits associated with neurological disorders
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction
  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus
  • previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
  • Our findings indicate that curcumin counteracted the TBI-related reduction in n-3 DPA.
  • curcumin may promote the conversion of n-3 DPA to DHA
  • the combination of both nutrients has been reported to produce anti-inflammatory action
  • the enhanced actions of curcumin and DHA in reducing cholesterol levels could be interpreted as preservation of levels of phospholipids in the plasma membrane
  • curcumin and DHA may contribute to reduce inflammation associated with the action of cholesterol in the pathology of TBI.
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    Curcumin and DHA shown to protect against TBI through a reduction in inflammation and maintenance of brain phospholipid membranes.  BDNF is increases also.
Nathan Goodyear

Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

  • strategies directed to preserve phospholipids in the plasma membrane such as the use of dietary docosahexaenoic acid (C22:6n-3; DHA)5 can have beneficial effects for post-TBI recovery
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction.
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  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • There was a significant group effect on BDNF (F 4,25 = 5.229, P < .01 by ANOVA), and FPI reduced BDNF levels (50% of CTL, P < .01; Figure 1C), which was counteracted by DHA supplementation (90% of CTL, P < .05; Figure 1C). Curcumin also counteracted this reduction of BDNF
  • The combination of curcumin and DHA had a trend of greater effects in BDNF (117% of CTL; Figure 1C) compared with DHA or curcumin alone.
  • curcumin contributed to enhance the action of DHA, protecting against cognitive impairment, and these effects were associated with elevations in the BDNF receptor signaling
  • Our current results show that curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus.
  • previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
  • The effects of the DHA diet and curcumin on cognitive enhancement were consistent with enhanced elevations in BDNF receptor signaling
  • effects of DHA and curcumin up to 2 weeks after TBI because this is the most critical period for the course of injury recovery because the brain is metabolically dysfunctional during this time
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    study that finds curcumin + DHA increased cognitive improvement after TBI within 2 weeks.  Good discussion of the proposed mechanism--increased BDNF.
Nathan Goodyear

Gut microbiota and non-alcoholic fatty liver disease: new insights - Aron-Wisnewsky - 2013 - Clinical Microbiology and Infection - Wiley Online Library - 0 views

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    gut microbiome plays a role in metabolic syndrome, IR and it should come as no surprise--NAFLD
Nathan Goodyear

Parental Dietary Fat Intake Alters Offspring Microbiome and Immunity - 0 views

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    What legacy do you leave your children?  Study finds that the "lard legacy" is one many leave their children.  Adults with high fatty acid profile, found in SAD, but this leaves alter gut microbiome in their children.
Nathan Goodyear

Effects of ethyl-eicosapentaenoic acid omega-3 fat... [Menopause. 2009 Mar-Apr] - PubMed result - 0 views

  • Effects of ethyl-eicosapentaenoic acid omega-3 fatty acid supplementation on hot flashes and quality of life among middle-aged women: a double-blind, placebo-controlled, randomized clinical trial.
  • Supplementation with E-EPA omega-3 fatty acid reduced HF frequency and improved the HF score relative to placebo
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    omega-3 aids in hot flash relief
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