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Nathan Goodyear

Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic O... - 0 views

www.ncbi.nlm.nih.gov/...PMC3198091

prebiotics probiotic Bifidobacterium leptin resistance leptin glucose lipids inflammation LPS

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    prebiotics found to increase leptin sensitivity, improved glucose metabolism, lipid metabolism, reduced inflammation and improved leaky gut.  The probiotics increased the bifidobacterium species versus a decrease in the Firmicutes phyla.
Nathan Goodyear

http://www.farm.ucl.ac.be/Full-texts-FARM/Delzenne-2010-3.pdf - 0 views

www.farm.ucl.ac.be/...Delzenne-2010-3.pdf

metabolic endotoxemia metabolic syndrome metabolic syndrome inflammation probiotics probiotic prebiotics prebiotic

shared by Nathan Goodyear on 11 Sep 14 - No Cached
  • Nathan Goodyear on 11 Sep 14
     
    Good review of metabolic endotoxemia, inflammation, and the use of probiotics, prebiotics to reduce inflammation and effect energy balance.  Implications in metabolic syndrome.
Nathan Goodyear

Prebiotics: The Concept Revisited - 0 views

jn.nutrition.org/...830S.full

prebiotics

shared by Nathan Goodyear on 11 Nov 14 - No Cached
  • Nathan Goodyear on 11 Nov 14
     
    prebiotics
Nathan Goodyear

Synbiotic supplementation in nonalcoholic fatty liver disease: a randomized, double-bli... - 0 views

ajcn.nutrition.org/...535.abstract

NAFLD non-alcoholic fatty liver synbiotics probiotic probiotics synbiotic fatty

shared by Nathan Goodyear on 18 Mar 14 - No Cached
  • Nathan Goodyear on 18 Mar 14
     
    small pilot study finds that synbiotics, probiotics and prebiotics, + lifestyle modifications work better than lifestyle modifications alone in NAFLD.
Nathan Goodyear

Targeting the Human Microbiome With Antibiotics, Probiotics, and Prebiotics: Gastroente... - 0 views

www.gastrojournal.org/...abstract

probiotics prebiotics antibiotics gut health dysbiosis metagenomics ASD autism

shared by Nathan Goodyear on 22 Oct 11 - No Cached
  • Nathan Goodyear on 22 Oct 11
     
    Gut health is in many ways were it all starts
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
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LeanBiome™ (Official) | Get Save UpTo $540 Today Only! - 0 views

usleanbiome.com

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shared by fitspresso on 27 Sep 23 - No Cached
  • fitspresso on 27 Sep 23
     
    LeanBiome™ (Official) | Get Save UpTo $540 Today Only! usleanbiome.com LeanBiome™ Hurry Up! Offer Expires in: 00 HOUR 29 MINUTE 59 SECOND LeanBiome Attention! Get Special 84% Discount Today Faster fat burning and weight loss Healthy cholesterol and sugar levels Higher energy levels Regular price: $129 Only for: 39$ What Is LeanBiome? LeanBiome Lean for Good is a weight loss dietary supplement derived from scientifically researched ingredients and comprehensively developed to help people achieve sustainable weight control. The formula comes in a capsule format that is easy to take and is made with natural ingredients from plants and other sources to achieve its goals. The main ingredient in LeanBiome is piperine, which has been found to affect the body's ability to absorb micronutrients and other compounds more effectively. LeanBiome is a dietary supplement that claims to help weight management. It contains 100% natural ingredients that support healthy weight loss. It does not interfere with any natural process making it safe for use. It ranks among the top weight loss supplements that claim to provide a permanent solution. LeanBiome is made by a company named Lean for Good. It is made with natural and research-backed ingredients that help you lose excess fat without hassles. It is sold in capsule form. The company assures the composition is GMO, gluten, and soy-free. As for manufacturing standards, you need not fret. The company makes the supplement in a facility certified by the FDA. How Does LeanBiome Work? The starting period of the LeanBiome program includes a detoxification process that effectively removes any accumulated ree radicals, toxins, fand oxidative stress. This cleansing enables improved blood circulation, setting the stage for the body to initiate its own fat-burning mechanisms. To enhance metabolic activity, introducing the lean bacteria contained in LeanBiome to your gut microbiome is a beneficial approach. This activation triggers r
Nathan Goodyear

The Gut Microbiota and Type 1 Diabetes - 0 views

www.ncbi.nlm.nih.gov/...PMC4761565

diabetes type I diabetes gut gut flora gut health gut microbiome gut microbiota dysbiosis

shared by Nathan Goodyear on 17 Oct 16 - No Cached
  • A study by Bosi and colleagues suggested that the increased gut permeability preceded the clinical onset of T1D
  • gut permeability may be an important player in the development of T1D but, as yet, the findings in human studies have shown association but causation will be more difficult to prove.
  • Early childhood (≤ 3 month) introduction to cereals [10, 11] and cow's milk [48] were shown to promote beta cell autoimmunity
  • ...1 more annotation...
  • These findings suggest that prebiotics and probiotics could be potential therapeutic tools to improve gut integrity in various intestinal inflammatory and autoimmune diseases including T1D
  • Nathan Goodyear on 17 Oct 16
     
    another great review article of gut dysbiosis, altered gut permeability and type I diabetes.
Nathan Goodyear

Targeting gut microbiota in obesity: effects of prebiotics and probiotics. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21826100

leptin leptin resistance obesity probiotics metabolic syndrome gut gut flora gut microbiota

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    Only abstract available here.  Review finds probiotics can be used in the arsenal to treat obesity and metabolic syndrome.  The authors conclude that leptin sensitivity is one of the possible mechanisms.
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...
  • high-fat diet induces metabolic endotoxemia in healthy individuals.
  • A link between energy intake (high-fat diet) and metabolic endotoxemia has also been described
  • associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
  • 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

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

Management of metabolic syndrome through probiotic and prebiotic interventions - 0 views

www.ncbi.nlm.nih.gov/...PMC3263193

probiotics probiotic metabolic syndrome metabolic syndrome

shared by Nathan Goodyear on 11 Sep 14 - No Cached
  • Nathan Goodyear on 11 Sep 14
     
    probiotic for metabolic syndrome.
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