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11beta-hydroxysteroid dehydrogenase type 1 an... [Front Horm Res. 2008] - PubMed - NCBI - 0 views

  • Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension
  • transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance
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    11-betaHSD1 expression and effect is site specific.
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Tissue-Specific Dysregulation of Cortisol Metabolism in Human Obesity - 0 views

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    dysregulated cortisol metabolism plays a role in obesity.  This study looked at obese men.  Decreased liver 11-betaHSD1 activity was found in the liver, with decreased cortisone to cortisol conversion.  Additionally, increase cortisol metabolites were found.  However, there was found to be an increase in 11-betaHSD1 activity in the adipose tissue increasing the cortisone to cortisol conversion indicating an increase in peripheral cortisol production.
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Body Fat Distribution and Cortisol Metabolism in Healthy Men: Enhanced 5β-Red... - 0 views

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    increased 11-betaHSD type 1 and increased 5-alpha reductase activity found to be associated with generalized obesity in men.  Both indicate increased cortisone to cortisol production.  
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Dehydroepiandrosterone reduces preadipocyte proliferation via androgen receptor - 0 views

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    DHEA reduces preadipocytes growth through the androgen receptor.
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Obesity - Dietary Capsaicin Reduces Obesity-induced Insulin Resistance and Hepatic Stea... - 0 views

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    This study looks at the effects of capsaicin on inflammation and obesity.  Capsaicin decreases IL-1B, IL-6, TNF-alpha and MCP-1.  This reduces insulin and leptin levels, as well as increase adiponectin activity.  This article also briefly discusses curcumin, which has similar activity.
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Web of Knowledge [v.5.3] - Web of Science - 0 views

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    human study: revealed a decrease in saturated fatty acids, omega-6 in those supplemented with DHEA-S.  DHEA-S was found to improve the metabolic profile of adipose tissue
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Insulin Up-Regulates Natriuretic Peptide Clearance Receptor Expression in the Subcutane... - 0 views

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    elevated insulin in insulin resistance decreases circulating Natriuretic peptide.  This provides a direct link between obesity and cardiovascular disease

The Best Ideal Home Fitness Equipment in Canada - 1 views

started by seofreelancer08 on 27 Jun 12 no follow-up yet
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Lose Body Fat: List of Super Green Foods - 0 views

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    Wheatgrass One example of those perfect food goods is wheatgrass. When broken down nutritionally, wheatgrass consists of more than twenty percent protein. This makes it a great supplement for folks who need more protein in their diet program, which includes a significant portion of the population.
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Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate... - 0 views

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    low-glycemic index diet aids in mobilization of adipose tissue in exercise.  In this study, exercise after a low-glycemic meal resulted in a greater mobilization of adipose tissue for energy production than a high glycemic meal.  This will help  in weight loss
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Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 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
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Adipose Tissue Inflammation in Obesity and Metabolic Syndrome - - Satoshi Nishimura - D... - 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.
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Obesity - Inducible Toll-like Receptor and NF-[kappa]B Regulatory Pathway Expression in... - 0 views

  • TLRs are functionally inducible and associated with downstream NF-B activation and proinflammatory cytokine production.
  • TLRs represent a family of receptors that are critical to the innate immune response against foreign pathogens and microorganisms
  • LPS has been shown to induce proinflammatory chemokine gene expression in differentiated human adipocytes through TLR and NF-B action
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  • Stimulation of TLRs initiates intracellular signaling cascades resulting in downstream NF-B and mitogen-activated protein kinase activation and production of proinflammatory chemokines associated with mechanisms of metabolic dysfunction and cardiovascular disease progression.
  • Elevated fatty acids levels associated with obesity activate TLR4 signaling in fat cells and macrophages, and induce insulin resistance in murine models
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    TLR, especially TLR-4, is directly involved in NF-KappaB activation and release of inflammatory cytokines
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Caloric restriction increases adiponectin expression by adipose tissue and prevents the... - 0 views

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    Calorie restriction increases adiponectin secretion from adipocytes.  Another plus of calorie restriction.  Remember, adiponectin and insulin are inversely associated.  Granted, this is in a rat model, but still supporting the overall health benefits of calorie restriction.
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Effects of novel capsinoid treatment on fatness and energy metabolism in humans: possib... - 0 views

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    Capsaicin shown to aid weight loss.
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Regulation of 11beta-HSD genes in human adipose tis... [Obes Res. 2004] - PubMed - NCBI - 0 views

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    adipocytes increase genetic expression of 11beta-HSD. This increases local cortisol production from cortisone.  This plays a pivotal role in obesity.  Question:  would this play a role in peripheral hypothyroid?  I think so.
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Growth hormone, insulin-like growth factor-I and th... [Horm Res. 2001] - PubMed - NCBI - 0 views

  • GH deficiency effectively increases cortisol production in key target tissues including liver and adipose tissue, promoting insulin resistance and visceral adiposity
  • GH/IGF-I modulation of cortisol metabolism may underpin the pathogenesis of common diseases such as central obesity
  • Patients with central obesity but with no evidence of hypopituitarism have relative GH deficiency and it is exciting to speculate that low-dose GH treatment in this group, by inhibiting cortisol generation within omental fat, may offer a novel therapeutic approach.
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    GH plays a key regulating role in obesity.  GH deficiency promotes increased cortisone to cortisol production in adipose tissue and liver.  This promotes insulin resistance and obesity. 
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Thermogenic ingredients and body weight re... [Int J Obes (Lond). 2010] - PubMed - NCBI - 0 views

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    Green tea is proposed to be a thermogenic compound that aids in weight loss.
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Antiobesity effects of green tea catechins: a... [J Nutr Biochem. 2011] - PubMed - NCBI - 0 views

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    green tea shown to add weight loss.  The physiologic mechanism discussed here in this study
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