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Nathan Goodyear

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

  • 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
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  • 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
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    Nice discussion of how diet, induces gut bacterial change, that leads to metabolic endotoxemia and disease.
Nathan Goodyear

Transkingdom Control of Microbiota Diurnal Oscillations Promotes Metabolic Homeostasis:... - 0 views

  • in addition to the type of diet being a modulator of microbiota composition, the timing of food intake plays a critical role in shaping intestinal microbial ecology.
  • the microbiota rhythms are influenced by the host clock and perform critical functions in the adaptation of metabolic processes to the diurnal fluctuations in the environment
  • Our study reveals that dysbiosis has a temporal dimension and that static microbiota comparisons might not be fully conclusive unless samples were taken in a controlled manner with respect to this important additional variable
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  • our taxonomic analysis indicates that microbiota oscillations are following rhythmic food intake
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    This is a really nice study.  Altered sleep-wake cycles result in altered food consumption which leads to altered gut microbiota diurnal oscillations.  Gut microbiota have a normal diurnal oscillation.  This altered gut flora then leads to increase insulin resistance, metabolic syndrome, diabetes...
Nathan Goodyear

BMC Microbiology | Full text | The Firmicutes / Bacteroidetes ratio of the human microb... - 0 views

  • The microbiota of the large intestine plays an important role in host metabolism and maintenance of host health
  • Our results defining a standard adult profile, together with previous reports, showed that C. leptum, C. coccoides, Bacteroides and Bifidobacterium represent the four dominant groups of the adult fecal microbiota
  • Sub-dominant groups are Lactobacilli Enterobacteriaceae, Desulfovibrio, Sporomusa, Atopobium as well as other bacterial groups including Clostridium clusters XI, XIVb, and XVIII
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  • In infant fecal microbiota, we observed Bifidobacterium as the dominant group
  • this observation is strongly related to diet, being enhanced by breast feeding
  • Significant higher numbers of Bifidobacterium were observed in infants versus adults and seniors
  • the gastrointestinal tract is first colonized by facultative anaerobes, such as E. coli
  • Strict anaerobes, such as Clostridium, colonize at later stages, as can be seen by the relatively low levels of C. leptum and C. coccoides in infants
  • diet change must be considered among the primary causes for such a shift of microbiota between infants and adults.
  • In the case of elderly subjects, our qPCR results indicated a significant increase in the counts of E. coli when compared to adults. This data is consistent with other publications indicating that elderly subjects harbor a different E. coli microbiota profile compared to younger adults
  • a number of authors reported a reduction in the numbers and diversity of many protective commensal anaerobes, such as Bacteroides and Bifidobacteria
  • The Firmicutes to Bacteroidetes ratio was already shown to be of significant relevance in signaling human gut microbiota status
  • Our measurements of the Firmicutes/Bacteroidetes ratio in adults obtained by our species-specific qPCR are in agreement with those obtained by Ley et al
  • Compared with young adults, the elderly have a different digestive physiology, characterized at a physiological level by a reduction in transit and of digestive secretions
  • The Firmicutes/Bacteroidetes ratio undergoes an increase from birth to adulthood and is further altered with advanced age
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    Good discussion of the gut microbiome.  Age effects the gut bacteria balance.  The Firmicutes/Bacteroidetes ratio increases from young, to young adult, to the elderly in this study.  Is this simply a reflection of aging or is the a biomarker that can be changed through diet and targeted probiotics?
Nathan Goodyear

Access : What are the consequences of the disappearing human microbiota? : Nature Revie... - 0 views

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    Changes in our gut microbiota are contributing to the health decline of Americans.  The mechanisms of this microbiota change is diverse.
Nathan Goodyear

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

  • 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
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  • 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
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    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

PLoS ONE: Influence of Milk-Feeding Type and Genetic Risk of Developing Coeliac Disease... - 0 views

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    fascinating article on how the environment and genetics play a role in the development of celiac disease.  In this study, the PROFICEL study, the intestinal microbiota was influenced by breast milk.  Those children breast fed had a favorable microbiota that decreased the incidence of celiac disease.
Nathan Goodyear

The Intestinal Microbiota Modulates the Anticancer Immune Effects of Cyclophosphamide - 0 views

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    Animal study finds that the chemo drug cyclophosphamide needs the gut microbiota to deliver the anticancer immune response.  Disruption of the gut microbiota will reduce this anti-cancer effect and render chemo less effective or worse even ineffective
Nathan Goodyear

PLOS ONE: The Gut Microbiota and Developmental Programming of the Testis in Mice - 0 views

  • The intra-testicular level of testosterone in GF mice was found to be significantly lower than in SPF and CBUT mice
  • This study establishes a novel role for the commensal gut microbiota in the regulation of testicular development and function
  • Absence of the normal microbiota influences the formation and the integrity of the BTB as well as the intra-testicular levels of testosterone and serum levels of LH and FSH.
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  • Nutritional, socioeconomic, lifestyle and environmental factors (among others) are involved in the regulation of normal spermatogenesis.
  • he gut microbiota is one such potential source of environmental factors/products that has developed an intimate symbiotic relationship with host's physiology.
  • Manipulation of the gut microbiotia through dietary modification, pre- and probiotics can therefore be beneficial for the host's reproductive health.
  • In the current study, colonizing GF mice with CBUT resulted in an increased sperm production, suggesting that bacterial products, e.g. of fermentation, directly or indirectly, can affect the testis.
  • the absence of gut microbiota influenced testosterone levels
  • A recent study demonstrated that dietary supplementation of the probiotics Lactobacillus reuteri increased and restored testosterone levels in aging mice
  • bacterial metabolites such as butyrate have been shown to increase the levels of LH [43] and FSH
  • This suggests that butyrate most likely regulates testosterone production at the testicular level by stimulation of gene expression in Leydig cells and with little or no effect at the pituitary- hypothalamic levels.
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    gut micro biome effects spermatogenesis, Testosterone production, and the brain-testicle-barrier.
Nathan Goodyear

The Firmicutes/Bacteroidetes ratio of the human microbiota changes with age | BMC Micro... - 0 views

  • C. leptum, C. coccoides, Bacteroides and Bifidobacterium represent the four dominant groups of the adult fecal microbiota
  • Lactobacilli Enterobacteriaceae, Desulfovibrio, Sporomusa, Atopobium as well as other bacterial groups including Clostridium clusters XI, XIVb, and XVIII
  • The Firmicutes/Bacteroidetes ratio undergoes an increase from birth to adulthood and is further altered with advanced age
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    good review/discussion of gut microbiota, including the firmicutes:bacteroidetes ratio.
Nathan Goodyear

Diet-Microbiota Interactions Mediate Global Epigenetic Programming in Multiple Host Tis... - 0 views

  • SCFAs play a dual role both as substrates for metabolism and as signaling molecules
  • SCFAs can be either directly converted (acetate) or oxidized (propionate and butyrate) to acetyl-Co
  • Here we demonstrate that microbial colonization regulates global histone acetylation and methylation in multiple host tissues in a diet-dependent manner
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  • complex functional interactions between diet, gut microbiota, and host health.
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    diet changes gut microbiota, which changes genetic expression--it is called epigenetics.  This is an animal study.
Nathan Goodyear

Colonization-Induced Host-Gut Microbial Metabolic Interaction - 0 views

  • he gut microbiota enhances the host’s metabolic capacity for processing nutrients and drugs and modulate the activities of multiple pathways in a variety of organ systems.
  • Acquisition of the gut microbiota was associated with rapid increase in body weight (4%) over the first 5 days of colonization
  • The colonization process stimulated glycogenesis in the liver prior to triggering increases in hepatic triglyceride synthesis
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  • modifications of hepatic Cyp8b1 expression and the subsequent alteration of bile acid metabolites
  • Expression and activity of major drug-metabolizing enzymes (Cyp3a11 and Cyp2c29) were also significantly stimulated
  • The gut microbiota (GM) exhibits a relatively low level of diversity compared to those of most soil ecosystems and in humans it is comprised of usually no more than nine phyla of microorganisms, of which only two are dominant: the Firmicutes and the Bacteroidetes
  • colonization of a germfree gut was rapid and remarkably stable, establishing within only a week after first exposure
  • a study conducted on germfree rats by Nicholls et al. showed that 3 weeks were necessary to obtain a stabilization and “normalization”
  • the microbiota status affects the systemic metabolism of the host, modulating the metabolic fingerprint of topographically remote organs such as the liver and the kidney
  • Gut colonization induces a rapid weight gain associated with stimulation of hepatic glycogenesis and triglyceride synthesis
  • Gut colonization alters bile acid metabolite profiles via modulation of hepatic Cyp8b1 expression
  • Bile acids are well-known contributors to glucose and lipid metabolism in the liver
  • GM is known to alter bile metabolism
  • GM is also known to exert a strong influence on the metabolism of xenobiotics
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    The effects of gut microbiome are not confined to the gut.  They alter bile acid metabolism and thus lipid/glucose metabolism.  They alter CYP450 activity.  They effect metabolism.  They effect the metabolism, and thus effects, of other drugs. 
Nathan Goodyear

Testosterone: More Than Having the Guts to Win the Tour de France - 0 views

  • female adult mice have microbiomes similar to those of prepubescent mice of both sexes;
  • the commensal microbial community in adult male mice significantly deviates from this shared initial pool.
  • the microbiome in castrated adult males clearly shifts away from that of normal adult males and is closer to the microbiome of females
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  • The incidence of T1D in these mice is positively correlated with the “femaleness” of the microbiota
  • These results support the hypothesis that the host androgen level is influential in determining the composition of the microbiota, which in turn affects T1D initiation and progression
  • a high testosterone level enriches the microbiota for specific organisms such as segmented filamentous bacteria (SFB) and Escherichia coli or Shigella–like (SECS) strains.
  • A minimum level of testosterone and specific male-enriched microbes working together upregulate M2 macrophage and IFN-γ producing T cells in pancreatic lymph nodes. Microarray data show that both the IFN-γ and IL-1β pathways are also stimulated.
  • These microbes also upregulate host testosterone
  • In four independent experiments, the authors found no universal unique “male microbiome”
  • they did find that four distinct combinations of microbial groupings (with an interesting lack of overlap at the individual family level in the four experiments) were enhanced by androgen
  • one species consists of the segmented filamentous bacteria (SFB) and belongs to the Firmicutes, whereas the other is an Escherichia coli or Shigella–like (SECS) strain belonging to the Proteobacteria
  • colonization with protective microbiomes—e.g., SPF microbiota, SFB, and SECS—is positively correlated with high blood testosterone levels in male mice
  • A direct implication of this study is that probiotic administration or fecal transplantation is a theoretically possible approach to protection against T1D
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    nice summary of article on the relationship between Testosteorne and gut microbiome in autoimmune disease.
Nathan Goodyear

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

  • 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
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  • 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.
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    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

Homeostasis in Intestinal Epithelium Is Orchestrated by the Circadian Clock and Microbi... - 0 views

  • a lack of microbiota results in a permanent ileal overproduction of corticosterone due to decreased expression of the D-box-binding E4BP4 repressor. This hypercorticosterolism generates systemic metabolic defects (hyperglycemia, insulin resistance, increased TG and FA)
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    to be read article on the communication between gut microbiota and intestinal epithelial cells and the resultant metabolic impact.
Nathan Goodyear

The role of short-chain fatty acids in the interplay between diet, gut microbiota, and ... - 0 views

  • Acetate, propionate, and butyrate are present in an approximate molar ratio of 60:20:20 in the colon and stool
  • SCFAs might play a key role in the prevention and treatment of the metabolic syndrome, bowel disorders, and certain types of cancer
  • SCFA administration positively influenced the treatment of ulcerative colitis, Crohn's disease, and antibiotic-associated diarrhea
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  • Gut bacteria in the cecum and large intestine produce SCFAs mainly from nondigestible carbohydrates that pass the small intestine unaffected
  • plant cell-wall polysaccharides, oligosaccharides, and resistant starches
  • inulin shifted the relative production of SCFAs from acetate to propionate and butyrate
  • age of approximately 3–4 years, when it becomes mature
  • SCFAs affect lipid, glucose, and cholesterol metabolism
  • colonocytes, the first host cells that take up SCFAs and which depend largely on butyrate for their energy supply
  • the microbiota educate the immune system and increase the tolerance to microbial immunodeterminants
  • the microbiota act as a metabolic organ that can break down otherwise indigestible food components, degrade potentially toxic food compounds like oxalate, and synthesize certain vitamins and amino acids
  • a large part of the SCFAs is used as a source of energy
  • The general idea is that colonocytes prefer butyrate to acetate and propionate, and oxidize it to ketone bodies and CO2
  • Exogenous acetate formed by colonic bacterial fermentation enters the blood compartment and is mixed with endogenous acetate released by tissues and organs (103, 104). Up to 70% of the acetate is taken up by the liver (105), where it is not only used as an energy source, but is also used as a substrate for the synthesis of cholesterol and long-chain fatty acids and as a cosubstrate for glutamine and glutamate synthesis
  • SCFAs regulate the balance between fatty acid synthesis, fatty acid oxidation, and lipolysis in the body.
  • Fatty acid oxidation is activated by SCFAs, while de novo synthesis and lipolysis are inhibited
  • obese animals in this study showed a 50% reduction in relative abundance of the Bacteroidetes (i.e., acetate and propionate producers), whereas the Firmicutes (i.e., butyrate producers) were proportionally increased compared with the lean counterparts.
  • increase in total fecal SCFA concentrations in obese humans.
  • In humans the distinct relation between the Firmicutes:Bacteroidetes ratio and obesity is less clear.
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    Great review of the role of SCFA in gut health and body metabolism
Nathan Goodyear

Prior Dietary Practices and Connections to a Human Gut Microbial Metacommunity Alter Re... - 0 views

  • Long-term DPs play a large role in determining the selective environment that the gut microbiota faces, ultimately influencing the composition and diversity of taxa maintained within the gut microbial community
  • Americans consuming unrestricted diets maintained less diverse fecal microbiota than those of individuals adhering to a plant-rich diet with restricted caloric intake
  • Experiments in mice have shown that multigenerational exposure to a Western diet poor in “microbiota-accessible carbohydrates” can lead to extirpation of specific bacterial lineages
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    Diet is the key to gut microbe diversity.  Gut microbes are key to maintaining optimal cellular metabolism.  Nutrition can be a prescription for improving and reprogramming gut bacteria.
Nathan Goodyear

Influence of mode of delivery on gut microbiota composition in seven year old children ... - 0 views

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    fascinating read.  This study looked at the mode of delivery and found that the balance of bifidobacterium and clostridium gut microbiota was altered by mode of delivery.  This has been associated with excessive IgE antibody production.  Ever wonder why we have so many allergies today?  Maybe it is because of the doctors rush to perform Ceserean Sections.
Nathan Goodyear

Involvement of gut microbiota in the developmen... [Gut Microbes. 2012] - PubMed - NCBI - 0 views

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    gut microbiota, and the imbalance of (dysbiosis) contributes to LPS and inflammation.  This results in obesity and type II DM.
Nathan Goodyear

Cell Host and Microbe - Microbiota Regulate Intestinal Absorption and Metabolism of Fat... - 0 views

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    You are what you eat...you are what your gut eats.  Confirmation of the influence of the GI microbiota on calorie utilization.   We shouldn't be surprised by this: what do we do to cattle?  we give them antibiotics which increases their weight and time to market.  What are we doing to ourselves?
Nathan Goodyear

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

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    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"
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