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Nathan Goodyear

Gut microbiota and non-alcoholic fatty liver disease: new insights - Aron-Wisnewsky - 2... - 0 views

onlinelibrary.wiley.com/...full

NAFLD gut gut flora gut microbiome gut microbiota metabolism non-alcoholic fatty liver LPS

shared by Nathan Goodyear on 05 Jul 15 - No Cached
  • Nathan Goodyear on 05 Jul 15
     
    gut microbiome plays a role in metabolic syndrome, IR and it should come as no surprise--NAFLD
Nathan Goodyear

Non-Alcoholic Fatty Liver Disease and Fructose: Bad for Us, Better for Mice - 0 views

www.ncbi.nlm.nih.gov/...PMC3117982

HCFS NAFLD high fructose corn syrup non-alcoholic fatty liver disease obesity overweight epidemic

shared by Nathan Goodyear on 19 Aug 11 - No Cached
  • Nathan Goodyear on 19 Aug 11
     
    great read on how HCFS has significantly contributed to the obesity epidemic and the new epidemic of NAFLD
Nathan Goodyear

Relationship between non-alcoholic fatty liver ... [World J Urol. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25189458

NAFLD BPH LUTS men male fatty liver liver metabolic syndrome

shared by Nathan Goodyear on 09 Sep 14 - No Cached
  • Nathan Goodyear on 09 Sep 14
     
    Men with NAFLD have higher incidence of lower urinary tract symptoms including BPH.
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

Probiotics and gut health: A special focus on liver diseases - 0 views

www.ncbi.nlm.nih.gov/...PMC2811790

probiotic probiotics liver cancer disease IBD IBS cirrhosis NAFLD gut health

shared by Nathan Goodyear on 05 Aug 14 - No Cached
  • Nathan Goodyear on 05 Aug 14
     
    Probiotics are not just for disease prevention, but also can be utilized as adjuncts for different liver disease states.  This review article highlights probiotics in IBD, IBS, surgery, NAFLD, cancer, and cirrhosis.
Nathan Goodyear

A low level of serum total testosterone is independently associated with nonalcoholic f... - 0 views

bmcgastroenterol.biomedcentral.com/...1471-230X-12-69

low Testosterone low T Testosterone NAFLD non-alcoholic fatty liver liver disease fatty liver hormones

shared by Nathan Goodyear on 16 Feb 16 - No Cached
  • Nathan Goodyear on 16 Feb 16
     
    low Testosterone is associated with NAFLD
Nathan Goodyear

N-Acetylcysteine Improves Liver Function in Patients with Non-Alcoholic Fatty Liver Dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3270338

NAC N-acetylcysteine NAFLD non-alcoholic fatty liver fatty liver liver enzymes

shared by Nathan Goodyear on 17 Jul 18 - No Cached
  • Nathan Goodyear on 17 Jul 18
     
    Oral NAC useful for elevated liver enzymes in NAFLD
Nathan Goodyear

Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views

jme.endocrinology-journals.org/...R51.full

metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation

shared by Nathan Goodyear on 04 Aug 14 - No Cached
  • Weight gain has been associated with a higher gut permeability
  • a high-fat diet promotes LPS absorption
  • higher concentrations of fatty acids impair intestinal barrier integrity
  • ...37 more annotations...
  • The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
  • TLRs are PRRs that recognize microbe-associated molecular patterns
  • TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
  • The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
  • Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
  • Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
  • LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
  • In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
  • In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
  • the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
  • dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
  • This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
  • n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
  • it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
  • this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
  • these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
  • This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
  • endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
  • in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
  • T2DM patients have mean values of LPS that are 76% higher than healthy controls
  • LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
  • LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
  • Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
  • The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
  • All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
  • LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
  • When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
  • It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
  • On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
  • high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
  • prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
  • Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
  • This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
  • high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
  • LPS has been shown to promote atherosclerosis
  • markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
  • As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
  • Nathan Goodyear on 04 Aug 14
     
    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

S-adenosylmethionine in alcoholic liver cirrhosis:... [J Hepatol. 1999] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...10406187

SAMe NAFLD GSH glutathione liver cirrhosis cirrhosis liver

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe, at doses of 1200 mg, shown to decrease mortality rate and prolong transplantation in those with cirrhosis.  Very likely, these individuals, if tested, had low SAMe and methyl donors as well as depleted glutathione. This is a set up for low phosphotidyl choline/ethanolamine levels resulting in fat accumulation.
Nathan Goodyear

JCI - Inflammatory links between obesity and metabolic disease - 0 views

www.jci.org/57132

obesity overweight weight-loss inflammation metabolic disease

shared by Nathan Goodyear on 04 Jan 12 - No Cached
  • metainflammation
  • The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
  • It is clear that inflammation participates in the link between obesity and disease
  • ...25 more annotations...
  • Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
  • adipose tissue macrophage (ATM)
  • Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
  • increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
  • The M2 activation state is intrinsically linked to the activity of PPARδ and PPARγ
  • well-known regulators of lipid metabolism and mitochondrial activity
  • Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
  • inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
  • Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
  • JNK, TLR4, ER stress)
  • NAFLD is associated with an increase in M1/Th1 cytokines and quantitative increases in immune cells
  • Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
  • DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
  • saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
  • Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
  • Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
  • Placental inflammation is a characteristic of maternal obesity
  • a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
  • Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
  • Nod-like receptor (NLR) family of PRRs
  • ceramides and sphingolipids
  • The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
  • adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
  • Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
  • NF-κB, obesity also activates JNK in insulin-responsive tissues
  • Nathan Goodyear on 04 Jan 12
     
    must read to see our current knowledge on the link between inflammation and obesity.
Nathan Goodyear

[Glutathione in the treatment of ch... [Recenti Prog Med. 1995 Jul-Aug] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...7569285

IV glutathione detoxification fatty liver disease NAFLD

shared by Nathan Goodyear on 10 Nov 11 - No Cached
  • Nathan Goodyear on 10 Nov 11
     
    high dose IV glutathione shown to reduce liver enzymes and thus liver cell damage in those with chronic fatty liver disease
Nathan Goodyear

Access : Nonalcoholic fatty liver disease: Microbiota in the pathogenesis of systemic a... - 0 views

www.nature.com/...nrendo.2012.25.html

fatty liver disease NAFLD non-alcoholic fatty liver inflammation dysbiosis metabolic

shared by Nathan Goodyear on 02 Aug 12 - No Cached
  • Nathan Goodyear on 02 Aug 12
     
    Fascinating read of how inflammation as a direct result of dysbiosis in the gut contributes to the progression of NALFD.
Nathan Goodyear

Probiotic as a Novel Treatment Strategy Against Liver Disease - Hepatitis Monthly - - K... - 0 views

hepatmon.com/?page=article&article_id=7521

probiotics liver disease cirrhosis hepatitis NAFLD non-alcoholic fatty liver

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    probiotics shown to be useful and safe in those with liver disease.
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

Epidemiology of non-alcoholic fatty liver disease. [Dig Dis. 2010] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...20460905

non-alcoholic liver fatty disease NAFLD obesity metabolic syndrome overweight

shared by Nathan Goodyear on 19 Aug 11 - No Cached
  • Nathan Goodyear on 19 Aug 11
     
    non-alcoholic fatty liver disease the result of Metabolic syndrome.  New epidemic associated with obesity. Scary statistics about the children of America.
Nathan Goodyear

The obesity epidemic and nonalcoholic fatty liver ... [Curr Gastroenterol Rep. 2008] - ... - 0 views

www.ncbi.nlm.nih.gov/...18417045

obesity epidemic NAFLD non-alcoholic fatty liver disease children

shared by Nathan Goodyear on 19 Aug 11 - No Cached
  • Nathan Goodyear on 19 Aug 11
     
    obesity and non-alcoholic fatty liver disease are one in the same.
Nathan Goodyear

Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic... - 0 views

onlinelibrary.wiley.com/...abstract

probiotics gut inflammation insulin glucose

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • these results support the concept that intestinal bacteria induce endogenous signals that play a pathogenic role in hepatic insulin resistance and NAFLD and suggest novel therapies for these common conditions.
  • Nathan Goodyear on 06 Apr 11
     
    Gut inflammation plays role in insulin/glucose dysregulation and inflammation
Nathan Goodyear

Nonalcoholic Fatty Liver Disease - 0 views

diabetes.diabetesjournals.org/...1844.short

nonalcoholic fatty liver disease metabolic syndrome

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • aracterized by clinical and laboratory data similar to those found in diabetes and obesity. NAF
  • We concluded that NAFLD, in the presence of normoglycemia and normal or moderately increased body weight, is ch
  • aracterized by clinical and laboratory data similar to those found in diabetes and obesity. NAF
  • ...1 more annotation...
  • LD may be considered an additional feature of the metabolic syndrome, with specific hepatic insulin resistance
  • Nathan Goodyear on 06 Apr 11
     
    Fatty Liver is component of Metabolic Syndrome
Nathan Goodyear

High Fructose Feeding Induces Copper Deficiency in... [J Hepatol. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21781943

fructose diet dietary Copper cu deficiency non-alcoholic fatty liver disease NAFLD

shared by Nathan Goodyear on 21 Oct 11 - No Cached
  • Nathan Goodyear on 21 Oct 11
     
    high Fructose dietary intake results in Copper deficiency.  Result is increase in non-alcoholic fatty liver.
Nathan Goodyear

http://ehp.niehs.nih.gov/wp-content/uploads/118/12/ehp.1002720.pdf - 0 views

ehp.niehs.nih.gov/...ehp.1002720.pdf

liver enzymes NAFLD liver disease cirrhosis hepatitis PCBs polychlorinated biphenyls Lead Pb Mercury Hg

shared by Nathan Goodyear on 22 Dec 14 - No Cached
  • Nathan Goodyear on 22 Dec 14
     
    PCBs, Lead, and Mercury associated with liver disease in American adults.  These possible causes need to be considered with non-explainable hepatitis.
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