androgen
deprivation therapy results in unfavorable changes in body composition, insulin resistance, and dyslipidemia and predisposes
men to develop atherosclerosis and an increased risk of cardiovascular mortality
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Association between circulating specific leukocyte types and blood pressure: the Athero... - 0 views
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Testosterone, the male hormone connection: treating diabetes and heart disease. - 0 views
www.worldhealth.net/...thera6_ch7.pdf
testosterone low T low testosterone CVD cardiovascular disease diabetes insulin leptin ghrelin PAI-1 obesity adiponectin type II diabetes DM atherosclerosis
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Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation o... - 0 views
www.jnutbio.com/...abstract
chylomicron inflammation atherosclerosis CAD arteriosclerosis plaque vascular disease
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Beyond the male sex hormone: deciphering the metabolic and vascular actions of testoste... - 0 views
joe.endocrinology-journals.org/...C1.full
AR androgen receptors androgen receptor testosterone androgen receptors Diabetes metabolic syndrome MetS CVD cardiovascular disease men hormone hormones male
shared by Nathan Goodyear on 08 May 13
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The hypogonadal–obesity cycle hypothesis was originally proposed by Cohen in 1999 to explain the relationship between low testosterone levels and metabolic disease. It was based on the finding that obesity impairs testosterone levels by increasing the aromatization of testosterone to estradiol, while low testosterone levels promote increased fat deposition
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adipocytokines contribute to low testosterone levels as well as to the processes underlying metabolic syndromes and type 2 diabetes
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The presence of estradiol and the adipocytokines TNF-α, IL6, and leptin (as a result of leptin resistance in obesity) inhibits the hypothalamic–pituitary–testicular axis response to decreasing androgen levels
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An increasing number of studies have illustrated the potential for applying metabolomics to the field of androgen research
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As early as the 1940s, the therapeutic use of testosterone was reported to improve angina pectoris in men with coronary artery disease
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most of the epidemiological studies reported increased cardiovascular risk and mortality in men with low testosterone levels
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long-term testosterone replacement appears to be a safe and effective means of treating hypogonadal elderly men
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a recent interventional trial showed that testosterone treatment was associated with decreased mortality when compared with no testosterone treatment in an observational cohort of men with low testosterone levels
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a number of short-term studies conducted support the notion that testosterone therapy reduces the cardiovascular risk
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The majority of animal studies support the hypothesis that the actions of testosterone on vascular relaxation are both endothelium-dependent and -independent vasodilatory effects
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Endothelial-dependent actions of testosterone increase the expression or activity of endothelial nitric oxide synthase and enhance nitric oxide production, which in turn activates cyclic guanosine monophosphate to induce vasorelaxation in smooth muscle cells
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Endothelial-independent mechanisms of testosterone are believed to occur primarily via inhibition of voltage-operated Ca2+ channels and/or activation of K+ channels in smooth muscle cells
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Testosterone may also inhibit intracellular Ca2+ influx via store-operated Ca2+ channels by blocking the response to prostaglandin F2α
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testosterone has demonstrated anti-inflammatory effects to protect against atherogenesis in animal studies
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both genomic AR activation to modulate gene transcription and non-genomic activation to modulate the rapid intracellular signaling pathways of ion channels may mediate testosterone effects on vascular function and inflammation.
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Butenandt & Ruzicka first showed how testosterone is synthesized and responsible for masculine characteristics in the early 1930s
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Understanding lipoproteins as transporters of cholesterol and other lipids - 0 views
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Two lipoprotein fractions are primarily involved in transport of lipid to peripheral tissues, very low density lipoproteins (VLDL) from the liver and chylomicrons from the intestinal tract
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As lipid is removed from these two fractions, the density of each fraction increases, thereby transforming VLDL into intermediate-density lipoprotein (IDL) and ultimately LDL, and chylomicrons into chylomicron remnants
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LDL-cholesterol has been described, and overly simplified, as “bad cholesterol” and HDL-cholesterol as “good cholesterol.”
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HDL, is primarily involved in returning lipid, largely cholesterol, to the liver in a process called reverse cholesterol transport
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Two primary subfractions of HDL have been classified as the higher-density HDL3, and the less dense, more lipid-filled HDL2
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Recent investigations are also suggesting that smaller, denser lipoproteins are associated with increased risk of atherosclerotic development
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Serum vitamin D and sex hormones levels in men and women: The Multi-Ethnic Study of Ath... - 0 views
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cross sectional study finds low vitamin D associated with a decrease in SHBG and an increase in free Testosterone; a decrease in estradiol and an increase in DHEA was seen in women. No association with total Testosterone was found. There are studies that show a direct decrease in testicular Testosterone production in men with low vitamin D and decrease in AR function.
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Amino Acid Intake Is Inversely Associated with Arterial Stiffness and Central Blood Pre... - 0 views
jn.nutrition.org/...jn.115.214700.abstract
amino acids protein cardiovascular cardiovascular disease health atherosclerosis
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Efficacy of Artichoke dry extract in patients with hyperlipoproteinemia. - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...10758778
artichoke artichoke extract natural alternative CYP450 cholesterol LDL atherosclerosis coronary heart disease
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The effect of supraphysiologic doses of test... [Atherosclerosis. 1997] - PubMed - NCBI - 0 views
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EDTA Chelation Therapy: A Retrospective Study of 470 Patients - 1 views
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Testosterone deficiency: A determinant of ao... [Atherosclerosis. 2014] - PubMed - NCBI - 0 views
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low Total Testosterone associated with CAD, particularly aortic. Obviously, Testosterone, when low, is a marker of poor health in men. However, low Testosterone can likely play a role in disease development, especially when age is factored in--low Testosterone in younger men likely plays an etiology versus a lesser impact in the elder.
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Nature Clinical Practice Endocrinology & Metabolism | Testosterone and ill-health in ag... - 0 views
www.nature.com/...ncpendmet1050.html
low T Testosterone health men male hormone hormones metabolic syndrome metabolic syndrome MetS insulin resistance diabetes aging
shared by Nathan Goodyear on 03 Mar 14
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Levels of total and bioavailable testosterone and SHBG were reported to be inversely correlated with the prevalence of the metabolic syndrome in men aged 40–80 years
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In longitudinal studies, decreased levels of total testosterone and SHBG predicted an increased incidence of metabolic syndrome in nonobese men
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Free testosterone level is not associated with the prevalence of metabolic syndrome in middle-aged and older men
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Levels of free, bioavailable and total testosterone are lower in men with T2DM than in age-matched controls,34, 35 and decreased total testosterone level predicts incident T2DM in middle-aged men.
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Total, bioavailable and free testosterone levels are inversely correlated with fasting insulin level and insulin resistance in middle-aged men without T2DM
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total testosterone is positively correlated with insulin sensitivity in men with normal or impaired glucose tolerance or T2DM
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low SHBG level is more strongly associated with metabolic syndrome than low total testosterone in aging men
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Low levels of SHBG are also associated with smaller, denser LDL-cholesterol molecules in nondiabetic men,58 and were found to predict increased cardiovascular disease mortality in one study of older men
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Compared with those who have normal testosterone levels, men aged 40 years or more with total testosterone levels <9.8 nmol/l or elevated LH level have greater CIMT
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a prospective analysis of men aged 73–91 years, progression of CIMT was not related to total testosterone level, but it was inversely related to free testosterone level
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A study of men aged 55 years or more found that those with total and bioavailable testosterone levels in the highest tertile had a lower risk of severe aortic atherosclerosis (detected by radiography as abdominal aortic calcification) than those with the lowest testosterone levels.
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a large study of men aged 69–80 years, those with total or free testosterone in the lowest quartile had increased odds of lower-extremity peripheral arterial disease
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the possibility of reverse causation has to be considered, as systemic illness can result in decreased testosterone levels
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previous case–control studies and longitudinal studies have failed to identify low testosterone levels as strong predictors of clinically significant coronary disease
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Reviews of trials on testosterone therapy in men with either low or low-to-normal testosterone levels have not shown consistent beneficial effects either on lipid profiles or on actual cardiovascular events.24, 54, 55 These trials, however, have not been designed or powered to detect treatment-related differences in cardiovascular outcome
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Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views
www.ncbi.nlm.nih.gov/...PMC3314172
metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation
shared by Nathan Goodyear on 09 Jul 13
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Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
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intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
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the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
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Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
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a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
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Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
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there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
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To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
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intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
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intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
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mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
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Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
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ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
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under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
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intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
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prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
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TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
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overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
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Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
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hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
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overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
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these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
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circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
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significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
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entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
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Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
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both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
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In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
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IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
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Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
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it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
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this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
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evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
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In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
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intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
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overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
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excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
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oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
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central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
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overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
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chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
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recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
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when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
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autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
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The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
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Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
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Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
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TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
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these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
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TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
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central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
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cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
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central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
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the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
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Low plasma testosterone and elevated carotid... [Atherosclerosis. 2012] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...22658553
low T Testosterone CRP CVD carotid IMT inflammation male men hormone hormones
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Low testosterone level as a predictor of cardiovascular events in Japanese men with cor... - 0 views
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Fructosamine and glycated albumin for risk stratification and prediction of incident di... - 0 views
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Serum and Dietary Potassium and Risk of Incident Type 2 Diabetes: The Atherosclerosis R... - 0 views
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Effects of gut microbiota on obesity and atherosclerosis via modulation of inflammation... - 0 views
onlinelibrary.wiley.com/...full
gut gut flora gut microbiome gut microbiota inflammation metaboliism
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Coenzyme Q10: a review of its promise as a neuropr... [CNS Spectr. 2007] - PubMed result - 0 views
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Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury.