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Nathan Goodyear

Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons - 0 views

www.ncbi.nlm.nih.gov/...PMC4523075

LPS lipopolysaccharides leptin CCK cholecystokinin metabolism weight appetite diet nutrition inflammation

shared by Nathan Goodyear on 04 Oct 17 - No Cached
  • Obesity and models of obesity induced by ingestion of HF-diet in rodents are associated with chronically elevated circulating levels of LPS
  • chronic low-dose administration of LPS induces leptin-resistance in vagal afferent neurons and abolition of CCK-induced inhibition of food intake
  • HF fat feeding has been shown to enhance gastrointestinal permeability promoting the translocation of LPS to the circulation
  • ...9 more annotations...
  • LPS leads to an increase in SOCS3 expression [20]. SOCS3 is a negative regulator of leptin signaling
  • We observed a significant increase in energy intake in the LPS-treated rats
  • the data provides a mechanism linking changes in gut microbiota induced by ingestion of HF diets to dysregulation of food intake and body weight
  • SOCS3 is an important mechanism by which leptin resistance develops in vagal afferent neurons and coincides with the onset of hyperphagia
  • Chronic low-dose LPS treatment induced TLR4 activation and MyD88 signaling in vagal afferent neurons, associated with increased SOCS3 expression and reduced leptin-signaling, characterized by the absence of leptin-induced pSTAT3.
  • We demonstrate that this chronic low dose LPS is sufficient to induce leptin–resistance in vagal afferent neurons, reduced sensitivity to the satiating effects of CCK, and loss of vagal afferent plasticity
  • it suggests that the increase in food intake and body weight we observed at week 6 in the LPS treated rats may be caused by LPS-induced leptin resistance.
  • chronic LPS treatment of mice for four weeks increased body weight
  • chronic LPS treatment of mice for four weeks increased subcutaneous fat
  • Nathan Goodyear on 04 Oct 17
     
    Very interesting study.  High fat diet in rats induced gut flora change that resulted in LPS which induced appetite through leptin resistance and reduced cholecystokinin signaling.
Nathan Goodyear

SARS-CoV-2 spike protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity - 0 views

www.ncbi.nlm.nih.gov/...PMC7799037

COVID SARS-CoV-2 COVID19 inflammation spike protein COVID-19 lipopolysaccharides LPS

shared by Nathan Goodyear on 21 Aug 21 - No Cached
  • Nathan Goodyear on 21 Aug 21
     
    SARS-CoV-2 spike protein works synergistically with LPS to stimulate inflammation via TLR4 receptors.
Nathan Goodyear

The effect of lipopolysaccharide-induced obesity and its chronic inflammation on influenza virus-related pathology - ScienceDirect - 0 views

www.sciencedirect.com/...S1382668915300983

obesity influenza lipopolysaccharides metabolic endotoxemia virus LPS

shared by Nathan Goodyear on 19 Sep 21 - No Cached
  • Nathan Goodyear on 19 Sep 21
     
    Study suggests LPS mediated obesity increases pathogenicity of influenza virus.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...22572877

microbiota flora dysbiosis LPS lipopolysaccharides inflammation obesity IR insulin resistance type II DM

shared by Nathan Goodyear on 05 Sep 12 - No Cached
  • Nathan Goodyear on 05 Sep 12
     
    gut microbiota, and the imbalance of (dysbiosis) contributes to LPS and inflammation.  This results in obesity and type II DM.
Nathan Goodyear

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

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • 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
  • ...25 more annotations...
  • 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
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

Cordycepin Suppresses Expression of Diabetes Regulating Genes by Inhibition of Lipopolysaccharide-induced Inflammation in Macrophages - 0 views

www.ncbi.nlm.nih.gov/...PMC2803303

cordyceps LPS inflammtion obesity DM Diabetes IL-1beta IL-6 TNF-alpha NF-KappaB

shared by Nathan Goodyear on 19 Jan 12 - No Cached
  • Nathan Goodyear on 19 Jan 12
     
    cordyceps shown to decrease LPS stimulated macrophage inflammation.  Specifically, IL-1Beta, IL-6, TNF-alpha were shown to be inhibited.  Also, NF-kappaB inhibition was found with cordyceps
Nathan Goodyear

Histochemistry and Cell Biology, Volume 127, Number 2 - SpringerLink - 0 views

www.springerlink.com/...yj35n4j531j67211

TLR TLR-4 toll-like receptors inflammtion obesity LPS lipopolysaccharides

shared by Nathan Goodyear on 19 Jan 12 - No Cached
  • Nathan Goodyear on 19 Jan 12
     
    Abstract only, but this study shows that the innate immunity plays a role in the development of obesity through the TLR.  LPS was shown to stimulate the inflammatory cascade through the TLRs
Nathan Goodyear

Low Doses of Lipopolysaccharide and Minimally Oxidized Low-Density Lipoprotein Cooperatively Activate Macrophages via Nuclear Factor κB and Activator Protein-1 - 0 views

circres.ahajournals.org/...56.full

LPS oxidized LDL inflammation macrophages NF-KappaB AP-1 atherosclerosis CAD

shared by Nathan Goodyear on 26 Sep 12 - No Cached
  • Nathan Goodyear on 26 Sep 12
     
    LPS and minimal oxidized LDL have synergistic effects on inflammatory signaling.  Together the two promote inflammatory signaling from macrophages at much lower levels than either one alone.  They do this through macrophage NF-KappaB and AP-1 pathways.  And this resultant inflammation promotes atherosclerosis.  Where does all this start?  our diet and our gut.
Nathan Goodyear

Glucose and lipopolysaccharide regulate pro... [J Reprod Immunol. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24576416

PCOS polycystic ovarian syndrome androgens DHEA Testosterone women hormone hormones atherogenesis CAD obesity obese inflammation

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • Nathan Goodyear on 03 Mar 14
     
    elevated androgens (male hormones) correlated with low grade inflammation and atherogenesis in women with PCOS.  This was found more in those women that were obese.
Nathan Goodyear

Mortality of Candida albicans-infected mice is ... [J Infect Dis. 1995] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...7769289

LPS lipopolysaccharide Candida albicans endotoxin

shared by Nathan Goodyear on 22 Jul 13 - No Cached
  • Nathan Goodyear on 22 Jul 13
     
    LPS from gram negative E. coli worsens negative effects of Candida albicans on mice cells.
Nathan Goodyear

Candida Albicans and LPS - 0 views

www.microbialinfluence.com/candida.html

candida albicans LPS lipopolysaccharide autism

shared by Nathan Goodyear on 22 Jul 13 - No Cached
  • Nathan Goodyear on 22 Jul 13
     
    Candida and impact/effect in autism. LPS production levels worsen impact of Candida on these children with autism.
Nathan Goodyear

Ginsenoside Rg3 Alleviates Lipopolysaccharide-Induced Learning and Memory Impairments by Anti-Inflammatory Activity in Rats - 0 views

www.ncbi.nlm.nih.gov/...PMC3825202

RG3 inflammation brain memory learning ginsenoside panax ginseng panax ginseng TNF-alpha IL-1beta cox-2 cognition

shared by Nathan Goodyear on 10 Apr 14 - No Cached
  • Nathan Goodyear on 10 Apr 14
     
    Rat model induced inflammatory reaction in brain via LPS injection.  The result was impaired memory.  RG3 from panax ginseng was shown to reduce inflammation, TNF-alpha, IL-1beta, cox-2, thus improving memory and cognitive function.
Nathan Goodyear

Metabolic Effects of Dietary Fiber Consumption and Prevention of Diabetes - 0 views

jn.nutrition.org/...439.long

soluble insoluble fiber dietary diet nutrition diabetes

shared by Nathan Goodyear on 22 Oct 13 - No Cached
  • DF are highly complex substances that can be described as any nondigestible carbohydrates and lignins not degraded in the upper gut
  • Commonly, DF are classified according to their solubility in water, even though grading according to viscosity, gel-forming capabilities, or fermentation rate by the gut microbiota might be physiologically more relevant
  • Main sources of soluble DF are fruits and vegetables
  • ...8 more annotations...
  • n increased intake of total DF was inversely associated with markers of insulin resistance in several studies
  • consumption of insoluble DF increased whole body glucose disposal independent of changes in body weight in both short-term and more prolonged studies
  • Short-chain fatty acids (SCFA) such as acetate, propionate, and butyrate are produced by bacterial fermentation of indigestible DF polysaccharides in the colon
  • increased production of SCFA is assumed to be beneficial by reducing hepatic glucose output and improving lipid homeostasis
  • a high DF diet (oligofructose) reduced gram-negative bacterial content and body weight, whereas a high fat diet increased the proportion of a gram-negative bacterial lipopolysaccharides (LPS) containing microbiota in humans
  • Prospective cohort studies indicate that diets high in insoluble cereal DF and whole grains might reduce diabetes risk
  • soluble DF (i.e., pectin, inulin, and β-glucans)
  • cereal DF (i.e., cellulose and hemicelluloses)
  • Nathan Goodyear on 22 Oct 13
     
    Good discussion of dietary fiber intake and Diabetes.  
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