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Nathan Goodyear

Diabetologia, Volume 46, Number 5 - SpringerLink - 0 views

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    This study finds obesity associated with inflammation, but insulin resistance not.  But insulin resistance contributes to obesity...
Nathan Goodyear

Access : Testosterone deficiency, insulin resistance and the metabolic syndrome : Natur... - 1 views

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    testosterone replacement in those with low T shown to improve insulin sensitivity, diabetes control, and metabolic syndrome in men.
Nathan Goodyear

Testosterone replacement therapy improves insulin resistance, glycaemic control, viscer... - 1 views

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    Testosterone therapy shown to improve insulin resistance, glucose control, hyperlipidemia, and aids weight loss in men with type II diabetes
Nathan Goodyear

Testosterone Concentrations in Women and Men With NIDDM - 1 views

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    insulin resistance has different effects in men versus women.  In men, insulin resistance is associated with low T in men, but in elevate T in women.
Nathan Goodyear

The Dark Side of Testosterone Deficiency: II. Type 2 Diabetes and Insulin Resistance --... - 1 views

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    low Testosterone associated with insulin resistance, type II diabetes, metabolic syndrome, and increased fat.  These will all translate to increased mortality.
Nathan Goodyear

Is central obesity, hyperinsulinemia and dyslipidemia associated with high-grade prosta... - 0 views

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    No surprise that insulin resistance, dyslipidemia, and obesity are associated with high-grade prostate cancer.  It's called inflammation.
Nathan Goodyear

Relationship Between Testosterone Levels, Insulin Sensitivity, and Mitochondrial Functi... - 0 views

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    Testosterone improves insulin resistance and mitochondrial function in those men with low Testosterone.
Nathan Goodyear

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity - 0 views

  • acute GC secretion during stress mobilizes peripheral amino acids from muscle as well as fatty acids and glycerol from peripheral fat stores to provide substrates for glucose synthesis by the liver
  • chronically elevated GC levels alter body fat distribution and increase visceral adiposity as well as metabolic abnormalities in a fashion reminiscent of metabolic syndrome
  • This local production may play an important role in the onset of obesity and insulin resistance.
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  • In adipocytes, cortisol inhibits lipid mobilization in the presence of insulin, thus leading to triglyceride accumulation and retention.
  • Since the density of GC receptors is higher in intra-abdominal (visceral) fat than in other fat depots, the activity of cortisol leading to accumulation of fat is accentuated in visceral adipose tissue (24, 158), providing a mechanism by which excessive endogenous or exogenous GC lead to abdominal obesity and IR
  • obese patients generally have normal or subnormal plasma cortisol concentrations
  • This may be explained by an increased intratissular/cellular concentration of cortisol in adipose tissues
  • Intracellular GC may be produced from recycling of GC metabolites such as cortisone in adipose tissues
  • Local GC recycling metabolism is mediated by 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2
  • Cortisol also increases 11β-HSD1 expression in human adipocytes
  • In humans, elevated 11β-HSD1 expression in visceral adipose tissue is also associated with obesity
  • even if obese patients generally have normal or subnormal plasma cortisol concentrations (131, 158), triglyceride accumulation in visceral adipose tissue may be due, at least in part, to the local production of GC in insulin- and GC-responsive organs such as adipose tissue, liver, and skeletal muscle
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    another nice article on the dysregulation of cortisol and its role in insulin resistance, metabolic syndrome, and obesity.
Nathan Goodyear

Obesity - Abstract of article: 11[beta]-Hydroxysteroid Dehydrogenase 2 Activity Is Elev... - 0 views

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    11-betaHSD type II increased in adipose tissue.  This correlates with insulin sensitivity.
Nathan Goodyear

Altered Cortisol Metabolism in Polycystic Ovary Syndrome: Insulin Enhances 5α... - 0 views

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    insulin, in women with PCOS, promotes increased 5-alpha reductase activity.  This results in a dysregulated HPA axis, promoting increased cortisol and androgen levels.
Nathan Goodyear

Hypoadiponectinemia in Obesity and Type 2 Diabetes: Close Association with Insulin Resi... - 0 views

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    obesity and type II diabetes found to be associated with low adiponectin and elevated insulin as found in insulin resistance.  This study revealed the inverse relationship of adiponectin and insulin resistance.  The interesting thing is that inflammation causes insulin resistance.  Here you can see the inflammation-insulin resistance-low adiponectin-obesity-diabetes link.
Nathan Goodyear

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.
Nathan Goodyear

Altered endocannabinoid signalling after a high... [Diabetologia. 2011] - PubMed - NCBI - 0 views

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    endocannaboid activation associated with inflammation, insulin resistance, and of course obesity.  This study was done in mice with a specific Apolipoprotein E deficiency.
Nathan Goodyear

Relationship of visceral adipose tissue and glucose disposal is independent of sex in b... - 0 views

  • an inverse nonlinear relationship existed between glucose disposal and visceral fat
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    Increase in visceral fat reduces glucose "disposal".  Translated: as visceral adiposity increases, associated insulin resistance increases glucose levels and all associated metabolic dysfunction.
Nathan Goodyear

Involvement of gut microbiota in the developmen... [Gut Microbes. 2012] - PubMed - NCBI - 0 views

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    gut microbiota, and the imbalance of (dysbiosis) contributes to LPS and inflammation.  This results in obesity and type II DM.
Nathan Goodyear

Hyperhomocysteinemia, deep vein thrombosi... [J Formos Med Assoc. 2007] - PubMed - NCBI - 0 views

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    Vitamin B12 deficiency will decrease methionine synthase activity, which will result in elevated homocysteine and the risk of DVT increases as a result.  In this article, the cause of the vitamin B12 depletion was metformin.  Diabetics and those with insulin resistance are already at an increased risk of blood clots.
Nathan Goodyear

Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fa... - 0 views

  • high-fat feeding strongly increased intestinal permeability and reduced the expression of genes coding for proteins of the tight junctions
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    changes in the gut flora shown to induce metabolic endotoxemia, inflammation, insulin resistance, and obesity.  Granted, this study was done in mice.
Nathan Goodyear

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
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • 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.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • 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

Plasma Adiponectin in Nonalcoholic Fatty Liver Is Related to Hepatic Insulin Resistance... - 0 views

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    in those with nonalcoholic fatty liver disease, low adiponectin is associated with the insulin resistance, not the NAFLD.  But of course, insulin resistance leads to NAFLD
Nathan Goodyear

JCI - Inflammation and insulin resistance - 0 views

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    How does inflammation cause insulin resistance?  This in-depth paper helps to explain the current understanding.   More and more obesity is part of a growing inflammatory epidemic.
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