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Nathan Goodyear

Targeting gut microbiota in obesity: effects of prebiotics and probiotics : Article : N... - 0 views

www.nature.com/...nrendo.2011.126.html

LPS lipopolysaccharides gut microbiota dysbiosis inflammation obesity metabolic endotoxemia health probiotics

shared by Nathan Goodyear on 18 Jan 12 - No Cached
  • gut microbes have a role in the host's metabolic homeostasis
  • lipopolysaccharide (LPS)
  • Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
  • ...8 more annotations...
  • associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
  • A link between energy intake (high-fat diet) and metabolic endotoxemia has also been described
  • high-fat diet induces metabolic endotoxemia in healthy individuals.
  • metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
  • A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
  • intestinal endocannabinoid system
  • The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
  • these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
  • Nathan Goodyear on 18 Jan 12
     
    good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity.  This article points to the presence of LPS playing a role in metabolic endotoxemia.  It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
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

Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fa... - 0 views

diabetes.diabetesjournals.org/...1470.full

metabolic metabolic endotoxemia obesity overweight LPS inflammation flora diet

shared by Nathan Goodyear on 29 Feb 12 - No Cached
  • Nathan Goodyear on 29 Feb 12
     
    2008 article from diabetes.  This article supports metabolic endotoxemia arising out of the gut.  High fat diet intake results in disrupted gut flora, resulting in increrased LPS release, resulting in inflammation, leads to leaky gut, systemic endotoxemia, inflammation, and thus metabolic dysfunction: see obesity, DM..
Nathan Goodyear

Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3448089

dysbiosis diet nutrition metabolic endotoxemia disease inflammation gut

shared by Nathan Goodyear on 27 Jul 14 - No Cached
  • The gut microbiota participates in the body’s metabolism by affecting energy balance, glucose metabolism, and low-grade inflammation associated with obesity and related metabolic disorders
  • Firmicutes and Bacteroidetes represent the two largest phyla in the human and mouse microbiota and a shift in the ratio of these phyla has been associated with many disease conditions, including obesity
  • In obese humans, there is decreased abundance of Bacteroidetes compared to lean individuals
  • ...21 more annotations...
  • weight loss in obese individuals results in an increase in the abundance of Bacteroidetes
  • there is conflicting evidence on the composition of the obese microbiota phenotype with regards to Bacteroidetes and Firmicutes ratios
  • Bifidobacteria spp. from the phyla Actinobacteria, has been shown to be depleted in both obese mice and human subjects
  • While it is not yet clear which specific microbes are inducing or preventing obesity, evidence suggests that the microbiota is a factor.
  • targeted manipulation of the microbiota results in divergent metabolic outcomes depending on the composition of the diet
  • The microbiota has been linked to insulin resistance or type 2 diabetes (T2D) via metabolic syndrome and indeed the microbiota of individuals with T2D is also characterized by an increased Bacteroidetes/Firmicutes ratio, as well as an increase in Bacillus and Lactobacillus spp
  • It was also observed that the ratio of Bacteriodes-Prevotella to C. coccoides-E. rectale positively correlated with glucose levels but did not correlate with body mass index [80]. This suggests that the microbiota may influence T2D in conjunction with or independently of obesity
  • In humans, high-fat Western-style diets fed to individuals over one month can induce a 71% increase in plasma levels of endotoxins, suggesting that endotoxemia may develop in individuals with GI barrier dyfunction connected to dysbiosis
  • LPS increases macrophage infiltration essential for systemic inflammation preceding insulin resistance, LPS alone does not impair glucose metabolism
  • early treatment of dysbiosis may slow down or prevent the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences
  • increased Firmicutes and decreased Bacteroidetes, which is the microbial profile found in lean phenotypes, along with an increase in Bifidobacteria spp. and Lactobacillus spp
  • mouse and rat models of T1D have been shown to have microbiota marked by decreased diversity and decreased Lactobacillus spp., as well as a decrease in the Firmicutes/Bacteroidetes ratio
  • microbial antigens through the innate immune system are involved in T1D progression
  • The microbiota appears to be essential in maintaining the Th17/Treg cell balance in intestinal tissues, mesenteric and pancreatic lymph nodes, and in developing insulitis, although progression to overt diabetes has not been shown to be controlled by the microbiota
  • There is evidence that dietary and microbial antigens independently influence T1D
  • Lactobacillus johnsonii N6.2 protects BB-rats from T1D by mediating intestinal barrier function and inflammation [101,102] and a combination probiotic VSL#3 has been shown to attenuate insulitis and diabetes in NOD mice
  • breast fed infants have higher levels of Bifidobacteria spp. while formula fed infants have higher levels of Bacteroides spp., as well as increased Clostridium coccoides and Lactobacillus spp
  • the composition of the gut microbiota strongly correlates with diet
  • In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp
  • diet has a dominating role in shaping gut microbiota and changing key populations may transform healthy gut microbiota into a disease-inducing entity
  • “Western” diet, which is high in sugar and fat, causes dysbiosis which affects both host GI tract metabolism and immune homeostasis
  • Nathan Goodyear on 27 Jul 14
     
    Nice discussion of how diet, induces gut bacterial change, that leads to metabolic endotoxemia and disease.
Nathan Goodyear

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

diabetes.diabetesjournals.org/...1470.full.pdf

dysbiosis obesity endotoxemia diabetes gut metabolic endotoxemia

shared by Nathan Goodyear on 15 Jan 13 - No Cached
  • Nathan Goodyear on 15 Jan 13
     
    This article discusses how an imbalance gut bacteria balance leads to endotoxemia and resultant obesity and diabetes. So, the balance of gut bacteria plays a role in obesity. Really changes ones view of how the body interacts and how disease develops through dysfunction.
Nathan Goodyear

Autism and Clostridium Tetani - 0 views

www.ncbi.nlm.nih.gov/pubmed

ASD autism metabolic endotoxemia children inflammation dysbiosis gut flora microbiota

shared by Nathan Goodyear on 30 Jan 12 - No Cached
  • Nathan Goodyear on 30 Jan 12
     
    Dysbiosis is commonly found in children with ASD. Antibiotics disrupt the normal gut microbiota resulting in dysbiosis. This imbalance in gut bacteria is now known to cause systemic inflammatory states such as metabolic endotoxemia. There is no reason to think a similar link may be present between Gut inflammation and ASD
Nathan Goodyear

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

diabetes.diabetesjournals.org/...db07-1403

gut microbiota flora metabolic endotoxemia inflammation insulin resistance IR obesity diabetes DM

shared by Nathan Goodyear on 18 Jan 12 - No Cached
  • high-fat feeding strongly increased intestinal permeability and reduced the expression of genes coding for proteins of the tight junctions
  • Nathan Goodyear on 18 Jan 12
     
    changes in the gut flora shown to induce metabolic endotoxemia, inflammation, insulin resistance, and obesity.  Granted, this study was done in mice.
Nathan Goodyear

The gut-liver-axis: Endotoxemia, inflammation, insulin resistance and NASH - 0 views

www.journal-of-hepatology.eu/...abstract

metabolic endotoxemia obesity overweight LPS bifidobacterium inflammaiton gut insulin resistance

shared by Nathan Goodyear on 20 Jan 12 - No Cached
  • Nathan Goodyear on 20 Jan 12
     
    metabolic endotoxemia starts with what you eat.  Chronic over nutrition results in elevated LPS. This starts a cascade of events that results in inflammation.  A well balanced gut flora of bifidobacterium is one way to slow this trigger.
Nathan Goodyear

Figure 2 : Targeting gut microbiota in obesity: effects of prebiotics and pro... - 0 views

www.nature.com/...nrendo.2011.126_F2.html

gut obesity probiotics metabolic endotoxemia LPS inflammation PPAR-gamma microbiota endocannabinoid system

shared by Nathan Goodyear on 18 Jan 12 - No Cached
  • Nathan Goodyear on 18 Jan 12
     
    nice diagram of proposed mechanism of how diet and gut microbiota can influence the production of PPAR-gamma inducing growth of adipose tissue.  Also proposes how LPS and the endocannabinoid system contributed to a leaky gut and thus the proposed "metabolic endotoxemia"
Nathan Goodyear

Colonic Microbiota Encroachment Correlates With Dysglycemia in Humans - Cellular and Mo... - 0 views

www.cmghjournal.org/...fulltext

'metabolic endotoxemia gut gut bacteria insulin resistance diabetes

shared by Nathan Goodyear on 12 Jun 17 - No Cached
  • most (86%) were overweight, many (45%) were obese
  • third (14 out of 42) had diabetes
  • in obese persons with diabetes, bacteria could be found in the dense inner mucus and in close proximity to the epithelium
  • Nathan Goodyear on 12 Jun 17
     
    Gut bacteria proximity, not just balance and diversity, to mucosa lining linked to systemic inflammation and insulin resistance in type II diabetes.  The role of type II diabetes may simply be the gut.  This has been called metabolic endotoxemia.
Nathan Goodyear

Metabolic endotoxaemia - a potential novel link between ovarian inflammation and impair... - 0 views

www.tandfonline.com/...09513590.2014.994602

metabolic endotoxemia progesterone hormones LPS lipopolysaccharides gut inflammation luteal phase defect

shared by Nathan Goodyear on 22 Jun 17 - No Cached
  • Nathan Goodyear on 22 Jun 17
     
    Systemic LPS, metabolic endotoxemia, that is the result of inflammation originating out of the gut found to cause luteal phase dysfunction--low progesterone.  Now, we have the gut-hormone connection.
Nathan Goodyear

Causative role of gut microbiota in non-alcoholic fatty liver disease pathogenesis - 0 views

www.ncbi.nlm.nih.gov/...PMC3481143

metabolic endotoxemia inflammation non-alcoholic fatty liver NAFLD gut bacteria fatty liver disease

shared by Nathan Goodyear on 14 Jan 13 - No Cached
  • Nathan Goodyear on 14 Jan 13
     
    metabolic endotoxemia plays role in NAFLD.  Gut bacterial balance plays a role in NAFLD.
Nathan Goodyear

Gut Microbiota in Health and Disease | Physiological Reviews - 0 views

physrev.physiology.org/...859

gut microbiota dysbiosis health GALT immune system LPS diet nutrition disease metabolic endotoxemia inflammation

shared by Nathan Goodyear on 27 Jul 14 - No Cached
  • Nathan Goodyear on 27 Jul 14
     
    Must read and a great read at that, of the GI's contribution to health or disease.  The article reviews the current understanding of the GALT layer and it's contribution to health or metabolic endotoxemia and how this then leads to disease. The article reviews the effects of disrupted GI bacteria in the gut as well as in other organ systems.
Nathan Goodyear

Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced d... - 0 views

dl-web.dropbox.com/...0DM%2C%20and%20endotoxemia.pdf

bifidobacterium flora LPS metabolic endotoxemia Diabetes DM type II obesity inflammation overweight weight-loss

shared by Nathan Goodyear on 20 Jan 12 - No Cached
  • Nathan Goodyear on 20 Jan 12
     
    decreased bifidobacterium gut flora results in increased absorption of LPS in high fat diets resulting in endotoxemia. This plays a significant role in diabetes
Nathan Goodyear

Dietary intervention impact on gut microbial gene richness : Nature : Nature Publishing... - 0 views

www.nature.com/...nature12480.html

gut bacteria dysbiosis obesity overweight diet nutrition metabolism metabolic endotoxemia

shared by Nathan Goodyear on 29 Aug 13 - No Cached
  • Nathan Goodyear on 29 Aug 13
     
    Nutrition is a language.  Poor gut balance and as what the authors call "richness" contributes to metabolic dysfunction and obesity.  This study found that Nutrition can improve gut bacterial balance and "richness" that then will improve the metabolic impact of the nutrition. Complex and beautiful nutrition--gut--metabolism connection.
Nathan Goodyear

Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syn... - 0 views

www.nature.com/...nature14232.html

metabolic syndrome metabolic endotoxemia gut flora gut microbiota processed foods probiotics microbiome gut inflammation obesity metabolism

shared by Nathan Goodyear on 01 Mar 15 - No Cached
  • Nathan Goodyear on 01 Mar 15
     
    Great article--only abstract available here.  Animal study finds that emulsifiers in process foods alters gut flora resulting in gut inflammation and obesity/metabolic syndrome.  Need an indictment against process foods--here you go.
Nathan Goodyear

PLOS ONE: High Fat Diet-Induced Gut Microbiota Exacerbates Inflammation and Obesity in ... - 0 views

www.plosone.org/...journal.pone.0047713

high fat diet inflammation metabolic endotoxemia metabolic syndrome obesity gut

shared by Nathan Goodyear on 14 Jan 13 - No Cached
  • Nathan Goodyear on 14 Jan 13
     
    good review of how diet increases inflammation through metabolic endotoxemia.  
Nathan Goodyear

Metabolic endotoxaemia related inflammation is associated with hypogonadism in overweig... - 0 views

www.ncbi.nlm.nih.gov/...PMC5341351

Testosterone low Testosterone Low T obesity IL-6 overweight metabolic endotoxemia hypogonadism LPS

shared by Nathan Goodyear on 06 Apr 17 - No Cached
  • Nathan Goodyear on 06 Apr 17
     
    Study finds that inflammation that is the result of obesity in men (IL-6) negatively effects the leading cell and Sertoli cells in men.  Testosterone levels in these men correlated significantly with lipopolysaccharide binding protein.  This points to a negative correlation b/t LPS metabolic endotoxemia and low Testosterone.  Could Testosterone merely be the result of an unhealthy diet and gut?
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