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Nathan Goodyear

Transaminase Levels and Vigorous Exercise - 0 views

www.ncbi.nlm.nih.gov/...PMC3104191

exercise liver enzymes

shared by Nathan Goodyear on 14 Mar 18 - No Cached
  • We accept 1–2 times the upper limit of normal to be attributable to exercise
  • Some physicians, whether they are gastroenterol-ogists or internists, forget that exercise can cause this abnormality
  • it is good for patients with liver disease to exercise, particularly those with fatty liver disease
  • ...4 more annotations...
  • we see a trend toward improved ALT and AST levels in patients performing moderate exercise, regardless of the etiology of their liver disease
  • We therefore discourage very heavy exercise in these patients, but a moderate amount does not cause a problem
  • once enzymes are abnormal, they remain abnormal for up to 1 week. Were subjects to exercise vigorously again during that week, transaminase levels could increase further
  • there is a ratio that in healthy individuals is considered normal. AST levels normally measure at approximately 0.8 of ALT levels. A dysregularity of this ratio can also signal hepatic illness but usually inflammation of any kind affects both measures
  • Nathan Goodyear on 14 Mar 18
     
    Vigorous exercise yields abnormal liver enzymes.  How one defines vigorous exericse is going to vary from person to person.
Nathan Goodyear

Anastrozole-related acute hepatitis with autoimmune features: a case report - 0 views

www.ncbi.nlm.nih.gov/...PMC3076249

anastrozole hepatitis autoimmune liver enzymes

shared by Nathan Goodyear on 08 Aug 16 - No Cached
  • Nathan Goodyear on 08 Aug 16
     
    anastrozole rarely associated with elevated liver enzymes.
Nathan Goodyear

The effectiveness of fermented turmeric powder in subjects with elevated alanine transa... - 0 views

www.ncbi.nlm.nih.gov/...PMC3600681

turmeric curcumin curcuma longa liver enzymes liver ALT astaxantin

shared by Nathan Goodyear on 06 Jul 16 - No Cached
  • Nathan Goodyear on 06 Jul 16
     
    fermented turmeric at 3 grams daily found to lower liver enzymes.
Nathan Goodyear

Environmental Health Perspectives: Polychlorinated Biphenyls, Lead, and Mercury Are Ass... - 0 views

ehsehplp03.niehs.nih.gov/...ehp.1002720

elevated enzymes ALT lead mercury PCBs heavy metals liver disease environmental health

shared by Nathan Goodyear on 05 Mar 12 - No Cached
  • Nathan Goodyear on 05 Mar 12
     
    Lead, Mercury, and PCBs shown to be a associated with elevations of liver enzymes, especially ALT.
Nathan Goodyear

Intratumoral androgen biosynthesis in prostate cancer pathogenesis and response to therapy - 0 views

erc.endocrinology-journals.org/...R175.full

prostate cancer DHT 3-beta-diol 3-alpha-diol metabolites metabolite male men hormone hormones androgen deprivation therapy

shared by Nathan Goodyear on 03 Feb 14 - No Cached
  • Additional studies have similarly found that prostate tissue levels of DHT in PCa patients treated with ADT therapy before prostatectomy declined by only ∼75% versus declines of ∼95% in serum levels
  • In a recent study in healthy men, treatment for 1 month with a GnRH antagonist to suppress testicular androgen synthesis caused a 94% decline in serum testosterone, but only a 70–80% decline in prostate tissue testosterone and DHT
  • progression to CRPC was associated with increased intratumoral accumulation or synthesis of testosterone.
  • ...9 more annotations...
  • the intraprostatic synthesis of testosterone from adrenal-derived precursors likely accounts for the relatively high testosterone levels in prostate after ADT
  • In addition, AR activity in these cells is likely further enhanced by multiple mechanisms that sensitize AR to low levels of androgens
  • higher affinity ligand DHT (approximately eightfold higher affinity
  • type 2 5α-reductase (SRD5A2) being the major enzyme in prostate
  • reduce DHT to 5α-androstane-3α,17β-diol (3α-androstanediol; Ji et al. 2003, Rizner et al. 2003), which is then glucuronidated to form 3α-androstanediol glucuronide by the enzymes UDP glycosyltransferase 2, B15 (UGT2B15) or UGT2B17
  • DHT in prostate is inactivated by the enzyme AKR1C2, which is also termed 3α-hydroxysteroid dehydrogenase type 3 (3α-HSD type 3
    • Nathan Goodyear
      Nathan Goodyear on 03 Feb 14
       
      The metabolite 3-alpha androstanediol is NOT inactive as this author states.  This DHT metabolite actually can stimulate  ER alpha receptors in the prostate.
  • AKR1C1, is also expressed in prostate. However, in contrast to AKR1C2, it converts DHT primarily to 5α-androstane-3β,17β-diol (3β-androstanediol; Steckelbroeck et al. 2004), which is a potential endogenous ligand for the estrogen receptor β
  • Significantly, intraprostatic testosterone levels were not substantially reduced relative to controls with normal serum androgen levels, although DHT levels were reduced to 18% of controls
  • testosterone levels in many of the CRPC samples were actually increased relative to control tissues (Montgomery et al. 2008). While DHT levels were less markedly increased, this may have reflected DHT catabolism
  • Nathan Goodyear on 03 Feb 14
     
    This article discusses the failure of androgen deprivation therapy and prostate cancer.  This failure is quite common.  The authors point to alpha-DHT as the primary mechanism through AR stimulation.  However, we know that DHT metabolites also stimulate estrogen receptors.
Nathan Goodyear

5α-reductase type 3 enzyme in benign and malignant ... [Prostate. 2014] - Pub... - 0 views

www.ncbi.nlm.nih.gov/...24150795

5 alpha reductase prostate cancer

shared by Nathan Goodyear on 06 Feb 14 - No Cached
  • Nathan Goodyear on 06 Feb 14
     
    3 subtypes of 5 alpha reductase enzymes identified in the human prostate.
Nathan Goodyear

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 - No Cached
  • 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
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • 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
  • ...56 more annotations...
  • 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
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • 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
  • 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
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • 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
  • 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
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • 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
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • 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.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • 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
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • 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
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • 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
  • 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
  • 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
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • 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
  • 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
  • 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
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • 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
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • 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
  • 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
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

AmeliorativeEffect ofVitaminC on Serum Liver Enzymes in Lead-Induced Toxicity in Wistar... - 0 views

www.dropbox.com/...IV%20vitamin%20C

IV vitamin C IV intravenous vitamin C hepatitis liver disease Pb toxicity

shared by Nathan Goodyear on 25 Sep 13 - No Cached
  • Nathan Goodyear on 25 Sep 13
     
    Study in Wistar Rats finds that IV vitamin C reduces the liver damage (manifested through elevated liver enzymes) associated with lead toxicity.
Nathan Goodyear

http://worldsciencepublisher.org/journals/index.php/JOS/article/viewFile/1186/899 - 0 views

worldsciencepublisher.org/...899

lead Pb IV vitamin C intravenous liver enzymes

shared by Nathan Goodyear on 31 Mar 14 - No Cached
  • Nathan Goodyear on 31 Mar 14
     
    IV vitamin C shown to decrease elevated liver enzymes in rat model of lead induced liver toxicity.
Nathan Goodyear

Polychlorinated Biphenyls, Lead, and Mercury Are Associated with Liver Disease in Ameri... - 0 views

www.ncbi.nlm.nih.gov/...PMC3002193

NAFLD liver enzymes disease non-alcoholic fatty liver PCBs Lead Mercury Hg Pb

shared by Nathan Goodyear on 31 Mar 14 - No Cached
  • Nathan Goodyear on 31 Mar 14
     
    full article that revealed PCBs, Lead, and Mercury associated with elevated liver enzymes and NAFLD.
Nathan Goodyear

Polychlorinated biphenyls, lead, and... [Environ Health Perspect. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21126940

PCBs polychlorinated biphenyls Pb Hg Mercury Lead liver enzymes damage NAFLD fatty

shared by Nathan Goodyear on 31 Mar 14 - No Cached
  • Nathan Goodyear on 31 Mar 14
     
    PCBs, Pb, and Hg associated with elevated liver enzymes, and non-alcohol fatty liver disease.  
Nathan Goodyear

Severe Starvation-Induced Hepatocyte Autophagy as a Cause of Acute Liver Injury in Anor... - 0 views

www.hindawi.com/...749169

liver enzymes anorexia malnutrition nutrition

shared by Nathan Goodyear on 20 Jul 15 - No Cached
  • Nathan Goodyear on 20 Jul 15
     
    extreme malnutrition as in anorexia is found to be associated with increased liver enzymes.
Nathan Goodyear

A case of amoxicillin-induced hepatocellular liver injury with bile-duct damage - 0 views

www.ncbi.nlm.nih.gov/...PMC3304646

amoxil amoxicillin liver antiobioitic liver enzymes

shared by Nathan Goodyear on 16 Apr 15 - No Cached
  • Nathan Goodyear on 16 Apr 15
     
    amoxil induced liver injury manifest with elevated liver enzymes.
Nathan Goodyear

Salivary cortisol determined by enzyme immunoassay... [Clin Endocrinol (Oxf). 2005] - P... - 0 views

www.ncbi.nlm.nih.gov/...16117823

saliva testing hormone salivary cortisol HPA axis

shared by Nathan Goodyear on 22 Nov 10 - No Cached
  • Nathan Goodyear on 22 Nov 10
     
    Salivary cortisol determined by enzyme immunoassay is preferable to serum total cortisol for assessment of dynamic hypothalamic--pituitary--adrenal axis activity.
Nathan Goodyear

The efficacy of licorice root extract in decre... [Phytother Res. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22308054

licorice licorice root extract NAFLD liver enzymes liver non-alcoholic fatty liver

shared by Nathan Goodyear on 10 Sep 14 - No Cached
  • Nathan Goodyear on 10 Sep 14
     
    Licorice root extract shown to reduce liver enzymes, significantly, but modestly in those with NAFLD.  The dose was 2 g daily.  The results occurred in just 2 months.
Nathan Goodyear

Long term administration of a licorice extract in the treatment of - 0 views

www.greenmedinfo.com/...patitis-c-effective-preventi-0

licorice licorice root extract liver enzymes liver cirrhosis liver Hepatitis C HCV hepatitis

shared by Nathan Goodyear on 10 Sep 14 - No Cached
  • Nathan Goodyear on 10 Sep 14
     
    Licorice root extract shown to significantly reduce liver enzymes in those with chronic hepatitis C and to prevent progression to liver cirrhosis.  
Nathan Goodyear

http://www.jgld.ro/2009/2/15.pdf - 0 views

www.jgld.ro/15.pdf

Lead lead toxicity liver enzymes

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • Nathan Goodyear on 09 Mar 15
     
    Lead toxicity associated with liver damage and elevated liver enzymes in case study.
Nathan Goodyear

http://maxwellsci.com/print/bjpt/v4-232-240.pdf - 0 views

maxwellsci.com/...v4-232-240.pdf

vitamin c liver enzymes Pb lead

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • Nathan Goodyear on 09 Mar 15
     
    Study finds vitamin C, vitamin E, Magnesium, selenium... associated with decreased negative effects elicited by Lead.  Lead has been shown to induce an elevation in liver enzymes and vitamin C has been shown to reduce this effect through its antioxidant activity.
Nathan Goodyear

Association of serum lead and mercury level with cardiometabolic ri... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25017868

ALT liver enzymes cholesterol blood pressure triglycerides metabolic syndrome lead Pb mercury Hg

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • Nathan Goodyear on 09 Mar 15
     
    study finds Pb and Hg associated with increased cardiometabolic risk factors.  Elevated liver enzymes found to be positively associated with serum Pb levels.  Metabolic Syndrome was found to be associated with higher Pb and Hg levels.
Nathan Goodyear

Unintended effects of statins from observational studies in the general population: sys... - 0 views

www.ncbi.nlm.nih.gov/...PMC3998050

statin therapy statins myopathy cholesterol side effects diabetes liver liver enzymes

shared by Nathan Goodyear on 19 Mar 15 - No Cached
  • A markedly increased risk of myopathy was observed
  • One cohort study (Women’s Health Initiative) of higher quality and larger sample size found stronger evidence of an increased risk of self-reported T2DM (OR=1.47; 95% CI 1.32 to 1.64) for the groups of women who reported statin use at baseline and three years later
  • Hippisley-Cox et al. found an increased risk of liver enzyme changes
  • ...5 more annotations...
  • weak evidence of an increased risk of type 2 diabetes mellitus (T2DM) was observed
  • Smeeth et al. found an increased risk of incident liver disease in the first year after the index date
  • The cumulative incidence of T2DM after three years of statin treatment was 6.25%, corresponding to an excess risk of 2.25%
  • We found no increased risk of peripheral neuropathy, depression, common eye diseases, renal disorders or arthritis associated with taking statins. Studies of higher quality did not show previously reported protective effects of statins on fractures, venous thrombo-embolism or pneumonia
  • There was evidence of an increase in myopathy, raised liver enzymes and diabetes.
  • Nathan Goodyear on 19 Mar 15
     
    Statin use associated with increased myopathy, liver dysfunction, and type II Diabetes.  The authors conclude that the absolute risk is very low, yet OR was 1.47 for type II Diabetes (translated 47% increased odds of developing Diabetes as a result of statins) and OR of 2.63 in risk of myopathy (translated 163% increased odds of developing myopathy as a result of statins).  Seems the authors "low risk" statement is just applies to those without symptoms/side effects.  Physicians need to do a better job of understanding risks and customizing therapies.
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