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Nathan Goodyear

Glutamic acid - Top 200 Food Sources of Glutamic acid | Top200Foods.com - 0 views

top200foodsources.com/Nutrients/Glutamic acid/515/g

glutamic acid glutamate MSG sources

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • Nathan Goodyear on 10 Feb 11
     
    Top 200 food sources of Glutamic Acid
Nathan Goodyear

Glutamate and the glutamate receptor system: a tar... [Int J Geriatr Psychiatry. 2003] ... - 0 views

www.ncbi.nlm.nih.gov/...12973748

glutamate glutamic acid excitotoxicity Parkinson's MS Alzheimer's Huntington's disease neurodegenerative

shared by Nathan Goodyear on 18 Mar 11 - No Cached
  • Under certain conditions, glutamate has a toxic action resulting from an activation of specific glutamate receptors, which leads to acute or chronic death of nerve cells.
  • Nathan Goodyear on 18 Mar 11
     
    deep, heavy read on glutamate excitotoxicity and neuronal death leading to neurodegenerative disease
Nathan Goodyear

Estrogen attenuates glutamate-induced cell death by inhibiting Ca2+ influx through L-ty... - 0 views

www.ncbi.nlm.nih.gov/...PMC2700344

estrogen estradiol apoptosis neurodegeneration glutamate glutamic acid

shared by Nathan Goodyear on 10 Mar 14 - No Cached
  • Nathan Goodyear on 10 Mar 14
     
    Estradiol inhibits glutamate mediated influx of calcium and thus cell death in cell line.  Glutamate, the principle excitatory neurotransmitter, is involved in neurodegeneration through activation of calcium channels.  This study of cell line cultures found that Estradiol inhibits this process.  I question whether this is applicable to both men and women.  Time will tell.
Nathan Goodyear

Brain glutamine and glutamate levels in patients with liver cirrhosis: assessed by 3.0-... - 0 views

www.sciencedirect.com/...S1386634604001330

glutamic acid glutamine glutamate brain liver

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    Brain glutamic acid originates from glutamine.  Glutamine should be avoided in those with excitotoxic diseases.
Nathan Goodyear

Exercise increases mitochondrial glutamate oxidation in the mouse cerebral cortex - App... - 0 views

www.nrcresearchpress.com/...apnm-2016-0033

exercise glutamate excitotoxicity glutamic acid brain

shared by Nathan Goodyear on 24 May 16 - No Cached
  • Nathan Goodyear on 24 May 16
     
    exercise found to reduce glutamate excitotoxicity in mouse study.
Nathan Goodyear

Pictorial Review of Glutamate Excitotoxicity: Fundamental Concepts for Neuroimaging - 0 views

www.ajnr.org/...1813.full

excitotoxicity Glutamate glutamic acid neurodegenerative disease Alzheimers Parkinsons ALS MS

shared by Nathan Goodyear on 13 Dec 11 - No Cached
  • Nathan Goodyear on 13 Dec 11
     
    excellent article on the imaging of excitotoxicity.  Glutamate excitotoxicity is a key component in neurodegenerative diseases: Alzheimers, Parkinsons, ALS, MS...
Nathan Goodyear

CNS Spectrums: Inflammation, Glutamate, and Glia in Depression: A Literature Review - 0 views

www.cnsspectrums.com/...articledetail.aspx

inflammation depression excitotoxicity glutamate glutamic acid mood disorders

shared by Nathan Goodyear on 20 Jan 12 - No Cached
  • Nathan Goodyear on 20 Jan 12
     
    inflammation, glutamate excitotoxicity and depression.  A very nice review of how inflammation can remotely contribute to other arenas of dysfunction, ie. depression.
Nathan Goodyear

Glutamate release promotes growth of malignant gli... [Nat Med. 2001] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11533703

glutamate glutamic acid MSG cancer glioblastoma multiforme

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • Nathan Goodyear on 10 Feb 11
     
    some tumors, glioblastoma multiforme, secrete glutamate, which increases aggressive nature of cancer
Nathan Goodyear

Creatine supplementation lowers brain glutamate levels in Huntington's disease. - PubMe... - 0 views

www.ncbi.nlm.nih.gov/...15672208

creatine Huntington's disease Huntington's excitotoxicity glutamate glutamic acid brain

shared by Nathan Goodyear on 21 Feb 16 - No Cached
  • Nathan Goodyear on 21 Feb 16
     
    Creatine helpful in decreasing glutamate levels in Huntington's disease.
Nathan Goodyear

Glutamate and its receptors in cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC4133641

glutamate glutamic acid cancer MSG

shared by Nathan Goodyear on 26 Feb 18 - No Cached
  • Nathan Goodyear on 26 Feb 18
     
    Glutamate, a common food additive that enhances flavor, is a growth factor for cancer.  
Nathan Goodyear

Press-pulse: a novel therapeutic strategy for the metabolic management of cancer | Nutr... - 0 views

nutritionandmetabolism.biomedcentral.com/...s12986-017-0178-2

ketogenic diet ketogenic press-pulse hyperbaric oxygen therapy HBOTnutrition diet cancer HBOT IVC IV vitamin C DCA dichloracetic acid cancer therapy cancer treatment alternative cancer treatment

shared by Nathan Goodyear on 09 Jul 17 - No Cached
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  • A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community
  • “pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality
  • Neoplasia involving dysregulated cell growth is the biological endpoint of the disease
  • ...84 more annotations...
  • Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
  • cancer is predicted to overtake heart disease as the leading cause of death in Western societies
  • cancer can also be recognized as a metabolic disease.
  • glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
  • Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
  • persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
  • Otto Warburg first proposed that all cancers arise from damage to cellular respiration
  • The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
  • the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
  • The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
  • Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
  • Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
  • all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
  • The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
  • respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
  • data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
  • Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
  • In addition to glucose, cancer cells also rely heavily on glutamine for growth and survival
  • Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
  • Glucose and glutamine act synergistically for driving rapid tumor cell growth
  • Glutamine metabolism can produce ATP from the TCA cycle under aerobic conditions
  • Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
  • Hif-1α stabilization enhances aerobic fermentation
  • targeting glucose and glutamine will deprive the microenvironment of fermentable fuels
  • Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
  • Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
  • Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
  • Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
  • Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
  • It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
  • Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
  • The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
  • According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
  • A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
  • Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
  • Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
  • The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
  • Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      reason to eliminate glutamine in cancer patients and even GSH with cancer patients
  • It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
  • Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
  • glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
  • In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
  • Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
  • Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
  • Ketone bodies and fats are non-fermentable fuels
  • Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
  • Apoptosis under energy stress is greater in tumor cells than in normal cells
  • A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
  • . This energy stress acts as a press disturbance
  • Drugs that target availability of glucose and glutamine would act as pulse disturbances
  • Hyperbaric oxygen therapy can also be considered another pulse disturbance
  • The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
  • Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
  • Protein amino acids can be metabolized to glucose through the Cori cycle
  • The fats in KDs used clinically also contain more medium chain triglycerides
  • Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
  • Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
  • GKI values of 1.0 or below are considered therapeutic
  • The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
  • It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
  • The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
  • Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
  • Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      Ketones are much more than energy adaptabilit, but actually are therapeutic.
  • ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
  • Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
  • Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
  • In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
  • Ketone supplementation has also been shown to reduce anxiety behavior in animal models
  • This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
  • lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
  • Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      oxaloacetate is a glycolytic inhibitor, as is doxycycline, and IVC.
  • A synergistic interaction of the KD diet plus radiation was seen
  • It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
  • Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
  • HBOT also increases oxidative stress and membrane lipid peroxidation of GBM cells in vitro
  • The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
  • Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
  • Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
  • Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
  • GBM and use glutamine as a major fuel
  • Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
  • Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
  • Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
  • Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
  • Nathan Goodyear on 09 Jul 17
     
    Cancer is a mitochondrial disease? So says the well published Dr Seyfried. Glucose and glutamine drive cancer growth.
Nathan Goodyear

Is administrating branched-chain amino acid-enriched nutrition achieved symptom-free in... - 0 views

www.ncbi.nlm.nih.gov/...PMC3882488

BCAA branched chain amino acids NH3 metabolism muscle glutamine glutamate glutamic acid liver cirrhosis disease nutrition

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    BCAA improve NH3 metabolism.  This is via muscle metabolism as reported in other studies.  This study highlighted the differences in BCAA supplementation.  One caveat is that high glutamine is the result from glutamate and this can increase hepatic encephalopathy.
Nathan Goodyear

Branched-chain amino acids and ammonia metabolism in liver disease: Therapeutic implica... - 0 views

www.sciencedirect.com/...S0899900713000907

BCAA branched chain amino acids glutamate glutamic acid glutamine alpha-ketoglutarate NH3 ammonia liver disease cirrhosis

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    BCAA are low in patients with liver cirrhosis due to increased glutamate production from glutamine.  The addition of BCAA in these patients is not without side effects--increased NH3 production.  The addition of alpha ketoglutarate should alleviate this risk.
Nathan Goodyear

Untitled Page - 0 views

www.cnsspectrums.com/...article_pf.aspx

inflammation glutamic acid glutamate glia astrocytes depression disordered tryptophan metabolism

shared by Nathan Goodyear on 14 Sep 11 - No Cached
  • Nathan Goodyear on 14 Sep 11
     
    review of inflammation, glutamic acid, glial activation and depression
Nathan Goodyear

Amino acid management in cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC4800996

amino acids cancer nutrition diet

shared by Nathan Goodyear on 15 Mar 19 - No Cached
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  • Nathan Goodyear on 15 Mar 19
     
    Serine, glycine, glutamine, glutamate, asparagine upregulated in cancer. Most glutamine is converted to glutamate to drive alpha-ketoglutarate production to drive energy production. It also upregulates mTOR signaling.
Nathan Goodyear

PLOS ONE: Depletion of Brain Docosahexaenoic Acid Impairs Recovery from Traumatic Brain... - 0 views

journals.plos.org/...article

DHA TBI traumatic brain injury omega 3 brain injury brain omega-3

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
  • LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
  • DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
  • ...10 more annotations...
  • DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
  • DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
  • AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
  • Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
  • severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
  • Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
  • it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
  • severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
  • DHA deficiency further elevates TBI-induced production of SBDPs
  • less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
  • Nathan Goodyear on 31 Aug 15
     
    mouse study finds prolonged recovery in DHA deficient mice compared to controls.
Nathan Goodyear

Ascorbate inhibits edema in brain slices. | Mendeley - 0 views

www.mendeley.com/...te-inhibits-edema-brain-slices

vitamin C excitotoxicity neurotoxin brain edema glutamate glutamic acid

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    vitamin C shown to reduce brain edema associated with glutamate excitotoxicity
Nathan Goodyear

We're Not "DON" Yet: Optimal Dosing and Prodrug Delivery of 6-Diazo-5-oxo-L-norleucine ... - 0 views

www.ncbi.nlm.nih.gov/...PMC6130910

glutamine DON dosing cancer

shared by Nathan Goodyear on 17 Mar 24 - No Cached
  • Glutamine is the most abundant amino acid in blood
  • Rapidly proliferating healthy cells (GI epithelium, lymphocytes) or cells under physiologic stress have increased demand for glutamine
  • Glutamine is transported into cells by one of multiple amino acid transporters (e.g. ASCT2, BOAT2), several of which are thought to be upregulated in cancer cells
  • ...10 more annotations...
  • it is hydrolyzed to glutamate and ammonia by glutaminase (‘glutaminolysis’)
  • Glutamate, produced from glutamine by glutaminase and glutamine amidotransferase activities, may be further metabolized to alpha ketoglutarate and provide a carbon skeleton source for the mitochondrial tricarboxylic acid cycle (TCA cycle)
  • Glutamine-derived glutamate is also involved in the synthesis of the reducing equivalent glutathione, vital to maintaining cellular redox status
  • Many tumors become largely dependent on glutamine to provide carbon and nitrogen building blocks needed for proliferation
  • In cancer model systems, Eagle and colleagues first demonstrated tumor cells in culture require supplementation with exogenous glutamine for efficient proliferation
  • It was subsequently shown that when deprived of glutamine tumor cells undergo apoptosis
  • The most well-characterized oncogene to regulate glutamine metabolism is MYC (9), which enhances glutaminase expression, upregulates glutamine transporters, and enhances glutamine utilization in energy production and biosynthesis
  • Other pro-tumorigenic regulators such as KRAS and mTOR, as well as tumor suppressors (p53, VHL) have also been associated with alterations in glutamine metabolism
  • Tumor cells are highly adaptable and alter nutrient uptake and metabolic networks to resist single agent glutaminase inhibition
  • cells in the microenvironment of several tumor types upregulate glutamine production, thereby enabling tumor cells to escape glutaminase inhibition
Nathan Goodyear

Hyperammonemia-induced depletion of glutamate and branched-chain am... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...8938556

ammonia NH3 BCCA branched chain amino acids glutamine

shared by Nathan Goodyear on 18 Nov 14 - No Cached
  • Nathan Goodyear on 18 Nov 14
     
    Elevated ammonia depletes glutamate and BCCA in muscle and plasma.  A decrease in BCCA is through an up regulation of glutamine in an attempt to eliminate ammonia.
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...PMC3735932

SCFA gut gut health diet nutrition metabolism gut flora gut microbiota

shared by Nathan Goodyear on 09 Nov 16 - No Cached
  • 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
  • ...16 more annotations...
  • 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.
  • Nathan Goodyear on 09 Nov 16
     
    Great review of the role of SCFA in gut health and body metabolism
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