Shortness of Breath (Dyspnea): Symptoms & Signs

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Lung Diseases Overview
Infections such as tuberculosis, mononucleosis, human immunodeficiency virus. During stage 2 intervention , they consumed milk supplemented with bifidobacteria for 3 wk. Mizushima N, Komatsu M. There are no adequate effectiveness or dose-response data for other pediatric conditions, but the experience in juvenile arthritis and other use experience have established that single doses of 2. The Disease is pheumothorax.

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Caffeine: how does it affect our health?

The increase in CV thrombotic risk has been observed most consistently at higher doses. To minimize the potential risk for an adverse CV event in NSAID-treated patients, use the lowest effective dose for the shortest duration possible.

Physicians and patients should remain alert for the development of such events, throughout the entire treatment course, even in the absence of previous CV symptoms.

Patients should be informed about the symptoms of serious CV events and the steps to take if they occur. There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. Observational studies conducted in the Danish National Registry have demonstrated that patients treated with NSAIDs in the post-MI period were at increased risk of reinfarction, CV-related death, and all-cause mortality beginning in the first week of treatment.

Although the absolute rate of death declined somewhat after the first year post-MI, the increased relative risk of death in NSAID users persisted over at least the next 4 years of follow-up. Avoid the use of Naproxen Suspension in patients with a recent MI unless the benefits are expected to outweigh the risk of recurrent CV thrombotic events. If Naproxen Suspension is used in patients with a recent MI, monitor patients for signs of cardiac ischemia. NSAIDs, including Naproxen, can cause serious gastrointestinal GI adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal.

These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. However, even short-term therapy is not without risk. Other factors that increase the risk of GI bleeding in patients treated with NSAIDs include longer duration of NSAID therapy; concomitant use of oral corticosteroids, aspirin, anticoagulants, or selective serotonin reuptake inhibitors SSRIs , smoking, use of alcohol, older age, and poor general health status.

Most postmarketing reports of fatal GI events occurred in elderly or debilitated patients. In addition, rare, sometimes fatal, cases of severe hepatic injury, including fulminant hepatitis, liver necrosis and hepatic failure have been reported.

Inform patients of the warning signs and symptoms of hepatotoxicity e. If clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur e. NSAIDs, including Naproxen Suspension, can lead to new onset of hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of CV events.

The Coxib and traditional NSAID Trialists' Collaboration meta-analysis of randomized controlled trials demonstrated an approximately two-fold increase in hospitalizations for heart failure in COX-2 selective-treated patients and nonselective NSAID-treated patients compared to placebo-treated patients.

Use of Naproxen may blunt the CV effects of several therapeutic agents used to treat these medical conditions [e. Avoid the use of Naproxen Suspension in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure.

If Naproxen Suspension is used in patients with severe heart failure, monitor patients for signs of worsening heart failure. Each 5 mL of Naproxen Suspension contains 39 mg of sodium. This should be considered in patients whose overall intake of sodium must be severely restricted.

Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. In these patients, administration of an NSAID may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation.

Patients at greatest risk of this reaction are those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors or ARBs, and the elderly. No information is available from controlled clinical studies regarding the use of Naproxen Suspension in patients with advanced renal disease. The renal effects of Naproxen Suspension may hasten the progression of renal dysfunction in patients with pre-existing renal disease.

Correct volume status in dehydrated or hypovolemic patients prior to initiating Naproxen Suspension. Avoid the use of Naproxen Suspension in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function. If Naproxen Suspension is used in patients with advanced renal disease, monitor patients for signs of worsening renal function.

Increases in serum potassium concentration, including hyperkalemia, have been reported with use of NSAIDs, even in some patients without renal impairment.

In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. When Naproxen Suspension is used in patients with preexisting asthma without known aspirin sensitivity , monitor patients for changes in the signs and symptoms of asthma. These serious events may occur without warning. Inform patients about the signs and symptoms of serious skin reactions and to discontinue use of Naproxen Suspension at the first appearance of skin rash or any other sign of hypersensitivity.

Naproxen may cause premature closure of the fetal ductus arteriosus. This may be due to occult or gross blood loss, fluid retention, or an incompletely described effect on erythropoiesis. If a patient treated with Naproxen Suspension has any signs or symptoms of anemia, monitor hemoglobin or hematocrit. Co-morbid conditions such as coagulation disorders, or concomitant use of warfarin, other anticoagulants, antiplatelet agents e.

Naproxen Suspension should not be used concomitantly with other Naproxen-containing products since they all circulate in the plasma as the Naproxen anion. Naproxen Suspension cannot be expected to substitute for corticosteroids or to treat corticosteroid insufficiency. Abrupt discontinuation of corticosteroids may lead to disease exacerbation.

Patients on prolonged corticosteroid therapy should have their therapy tapered slowly if a decision is made to discontinue corticosteroids and the patient should be observed closely for any evidence of adverse effects, including adrenal insufficiency and exacerbation of symptoms of arthritis. Patients with initial hemoglobin values of 10 g or less who are to receive long-term therapy should have hemoglobin values determined periodically.

Because of adverse eye findings in animal studies with drugs of this class, it is recommended that ophthalmic studies be carried out if any change or disturbance in vision occurs. Advise the patient to read the FDA-approved patient labeling Medication Guide that accompanies each prescription dispensed. Inform patients, families, or their caregivers of the following information before initiating therapy with Naproxen Suspension and periodically during the course of ongoing therapy.

Advise patients to be alert for the symptoms of cardiovascular thrombotic events, including chest pain, shortness of breath, weakness, or slurring of speech, and to report any of these symptoms to their healthcare provider immediately see WARNINGS; Cardiovascular Thrombotic Events.

Advise patients to report symptoms of ulcerations and bleeding, including epigastric pain, dyspepsia, melena, and hematemesis to their health care provider. Advise patients to be alert for the symptoms of congestive heart failure including shortness of breath, unexplained weight gain, or edema and to contact their healthcare provider if such symptoms occur see WARNINGS; Heart Failure and Edema. Inform patients of the signs of an anaphylactic reaction e.

Alert patients that NSAIDs may be present in "over the counter" medications for treatment of colds, fever, or insomnia. Caution should be exercised by patients whose activities require alertness if they experience drowsiness, dizziness, vertigo or depression during therapy with Naproxen.

The pharmacological activity of Naproxen in reducing inflammation, and possibly fever, may diminish the utility of diagnostic signs in detecting infections.

See Table 1 for clinically significant drug interactions with Naproxen. No evidence of tumorigenicity was found. Studies to evaluate the mutagenic potential of Naproxen Suspension have not been completed. Studies to evaluate the impact of Naproxen on male or female fertility have not been completed. Use of NSAIDs, including Naproxen Suspension, during the third trimester of pregnancy increases the risk of premature closure of the fetal ductus arteriosus.

Data from observational studies regarding potential embryofetal risks of NSAID use in women in the first or second trimesters of pregnancy are inconclusive. In the general U. In animal reproduction studies in rats, rabbit, and mice no evidence of teratogenicity or fetal harm when Naproxen was administered during the period of organogenesis at doses 0.

Based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, administration of prostaglandin synthesis inhibitors such as Naproxen, resulted in increased pre- and post-implantation loss. There is some evidence to suggest that when inhibitors of prostaglandin synthesis are used to delay preterm labor there is an increased risk of neonatal complications such as necrotizing enterocolitis, patent ductus arteriosus and intracranial hemorrhage.

Naproxen treatment given in late pregnancy to delay parturition has been associated with persistent pulmonary hypertension, renal dysfunction and abnormal prostaglandin E levels in preterm infants.

Because of the known effects of nonsteroidal antiinflammatory drugs on the fetal cardiovascular system closure of ductus arteriosus , use during pregnancy particularly starting at 30 weeks of gestation, or third trimester should be avoided. In animal studies, administration of prostaglandin synthesis inhibitors such as Naproxen, resulted in increased preand post-implantation loss.

There are no studies on the effects of Naproxen Suspension during labor or delivery. In animal studies, NSAIDS, including Naproxen, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth.

The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for Naproxen Suspension and any potential adverse effects on the breastfed infant from the Naproxen Suspension or from the underlying maternal condition. Based on the mechanism of action, the use of prostaglandin-mediated NSAIDs, including Naproxen Suspension, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women.

Published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin- mediated follicular rupture required for ovulation. Consider withdrawal of NSAIDs, including Naproxen Suspension, in women who have difficulties conceiving or who are undergoing investigation of infertility.. Safety and effectiveness in pediatric patients below the age of 2 years have not been established. There are no adequate effectiveness or dose-response data for other pediatric conditions, but the experience in juvenile arthritis and other use experience have established that single doses of 2.

Studies indicate that although total plasma concentration of Naproxen is unchanged, the unbound plasma fraction of Naproxen is increased in the elderly.

Caution is advised when high doses are required and some adjustment of dosage may be required in elderly patients. As with other drugs used in the elderly, it is prudent to use the lowest effective dose.

Experience indicates that geriatric patients may be particularly sensitive to certain adverse effects of nonsteroidal anti-inflammatory drugs.

Elderly or debilitated patients seem to tolerate peptic ulceration or bleeding less well when these events do occur. Naproxen is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.

Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function. Geriatric patients may be at a greater risk for the development of a form of renal toxicity precipitated by reduced prostaglandin formation during administration of nonsteroidal anti-inflammatory drugs see WARNINGS; Renal Toxicity and Hyperkalemia.

Medscape Reference [On-line information]. Medscape Medical News [On-line information]. Updated January 4. Updated May Hepatocellular Carcinoma. Mayo Clinic Staff January 22 Cirrhosis. Updated July Cirrhosis and Portal Hypertension. Merck Manual for Healthcare Professionals [On-line information]. Updated October MedlinePlus Medical Encyclopedia [On-line information]. Update October 4 Cirrhosis. American Liver Foundation [On-line information].

Contemporary Practice in Clinical Chemistry 2nd Edition: Send Us Your Feedback. Choose Topic What is cirrhosis? This article was last reviewed on January 18, This article was last modified on February 1, Some examples of these effects and complications include: An increase in pressure in the vein that carries blood to the liver; this is called portal hypertension.

Causes are wide-ranging but generally fall into one of several categories: Alcoholic—excessive alcohol use over time can lead to alcoholic liver disease and cirrhosis. Symptoms may be nonspecific and include: Both panels include the following tests: Alanine aminotransferase ALT — an enzyme found mainly in the liver. Values are increased with all types of liver injury, including cirrhosis.

Aspartate aminotransferase AST — an enzyme found in the liver and other organs. AST is elevated in people with liver injury, including cirrhosis.

Alkaline phosphatase ALP — an enzyme found along bile ducts. ALP is usually normal or mildly elevated in cirrhosis. Total bilirubin — a substance produced exclusively in the liver. It is increased with many liver diseases. Bilirubin is usually normal or slightly elevated until cirrhosis becomes far advanced.

Albumin — a protein made by the liver that is often decreased in cirrhosis. Other routine testing may include: This test evaluates clotting function and results may be prolonged with cirrhosis. Additional Testing Hepatitis B and hepatitis C testing may be ordered to help diagnose the underlying cause of chronic liver disease. If ascites is present, peritoneal fluid analysis may be performed. That includes fibre , but also microorganisms, and secretions and cells shed from the alimentary tract.

While there are studies that support the benefit of fibre in IBD, there are others showing harm. The evidence is mixed enough to be called weak and inconclusive [Kap]. Anecdotes such as the " Crohn's Carnivore " suggest a different solution might hold for some:. That experience runs both with and possibly against current dietary guidelines for IBD. In a review [Bro] , the authors show that most guidelines advise low fibre intake, especially during flares. Some also advise low fat intake, and in particular, to eat lean meat.

I'm not sure whether the Crohn's Carnivore was eating lean or fatty meat during his year of healing. At first blush, the low fat advisory looks like just another "extra-mile" kind of recommendation, in which guideline writers are throwing in other ideas about healthy diet for good measure. However, they state that it comes from the reported reactions of some patients. One wonders if there are conflations. Later, the authors specifically say that there is little to support or refute a low fat recommendation.

Another anecdote, this time elevated to "case study" level, because physicians penned it, comes from the Evolutionary Medicine Working Group, in Budapest, Hungary [Tot]. They report complete resolution of symptoms in a child with Crohn's and cessation of medications from an essentially meat-only diet.

The exception was that patient was allowed some honey, but it was low enough that ketosis was maintained. This was a 2: The child had previously tried low fat, low fibre, and several medications without improvement. It is interesting to note that even one dose of "paleo approved" fibre caused a flare up. In other words, a fibre-free ketogenic diet appears help IBD more than a diet including fibre, even a ketogenic diet including fibre.

The idea that butyrate might be protective of colon cancer seems to have started in the s see, e. This area of research is extensive, and I am by no means an expert. If you haven't guessed, that butyrate has a protective effect on colon cancer is the one statement I think is entirely defensible.

For example butyrate's histone deacelytase HDAC inhibition is considered an important mechanism [Hin] , [Blo]. Gpra receptor activation is a recently identified mechanism [Sin]. In fact, the argument behind the relevance of the Gpra discovery is just as strong an argument for a ketogenic diet as for eating fibre!

This sentence is incorrect. That is, the researchers demonstrated that butyrate could substitute for niacin in activating these receptors, and that just as niacin activation of Gpra in fat cells is protective of cardiovascular disease, it may also be in diseases of the colon, and this argues for eating fibre to substitute for pharmalogic doses of niacin. From a press release:.

Their search for other activators identified butyrate, which led Ganapathy to find that not only is the Gpra receptor expressed on the surface of colon cells, but that with sufficient fiber intake, butyrate levels in the colon can activate it. A critic pointed out that the cell receptors for SCFAs are facing the lumen, and therefore argued that beta-hydroxybutyrate from the portal side would be irrelevant.

Indeed, the researchers using niacin also assume that the extremely high dose of niacin does not act sytemically, but rather reaches the lumen because of the super-high doses. So the statement I made above, about the argument for beta-hydroxybutyrate being equal to that for niacin is not correct. The argument still stands that the beta-hydroxybutyrate metabolites activating targets inside could be where the majority of the benefits of butyate come from.

That is where the HDAC inhibition occurs and where the immune cell receptors are. At least one research group agrees with my speculation that the interior metabolites may be important for the effect [Siv].

SCFAs are low-affinity agonists for these receptors, and the normal luminal concentrations of these bacterial metabolites are in the millimolar levels, sufficient to activate these receptors from the luminal side. However, some of the molecular targets for these metabolites are either inside the cells e. Therefore, concentrations of these metabolites inside the colonic epithelial cells and in the lamina propria are relevant to impact these molecular targets.

The intracellular target HDAC is inhibited by butyrate and propionate at low micromolar concentrations. There are effective transport systems for SCFAs in the apical membrane of colonic epithelial cells e. Even though the luminal concentrations of SCFAs are in the millimolar range, it is unlikely that they reach lamina propria at significant levels to activate the cell-surface receptors present on the mucosal immune cells.

These metabolites are present only at micromolar levels in the portal blood [57], indicating that they undergo robust metabolism inside the colonic epithelial cells. This raises the question as to the physiological relevance of these bacterial metabolites to the activation of the cell-surface SCFA receptors in immune cells located in the lamina propria. This ketone body is released from the cells into portal blood.

Interestingly, as in the case of colitis, colorectal cancer appears to involve a dysfunction in ability to use butyrate. Specifically, there are detrimental changes in membrane transport that reduce its entry into the cell [Gon]. Therefore, it's unclear that once the disease process has begun, increased fibre intake will be of any use. Beta-hydroxybutyrate in the bloodstream, however, might. There is at least some preliminary evidence that butyrate in the bloodstream has similar effects on intestinal tissue as butyrate coming from the colon itself [Kor] , [Rol] , [Bar] , as does infusion of glutamine and acetoacetate, another ketone body [Rom].

Ketogenic diets do increase blood acetoacetate. These common mechanisms suggest that much or even all of the benefits obtainable by butyrate are equally achievable simply through ketogenic diets, making additional butyrate in the context of a ketogenic diet potentially superfluous.

Even though it seems likely that a fibre-free ketogenic diet is not only sufficient for colon health, but better for treating colon disease, we might feel cautious about going without the butyrate from fibre, given the dire pronouncements from nutritional scientists.

Is there any other way to get butyrate? The most significant food source, butter, doesn't give much. That would take about a pound of butter! Stepping back, it should be obvious that carnivores such as felines and canines provide an important source of data relevant to this question. Carnivores have colons, and they are not normally in ketosis unless food is scarce. Either their colons don't need butyrate, or they are getting sufficient butyrate from some other source.

As it happens, there are microbes that ferment amino acids in to short chain fatty acids SCFAs , including butyrate. Carnivores are known to get "animal fibre" from their prey. That is, amino acids from incompletely digested animal parts reach their colons and are fermented. In particular, in cheetahs, casein, collagen, and glucosamine have been shown to result in butyrate production comparable to fructo-oligosaccharides [Dep]. Beyond poorly digested animal sourced fibre, many amino acids are fermented into SCFAs, including butyrate [Ras] , and these amino acids are abundant in human intestines and colons and are fermented there [Vit] , [Dai] , [Nei] , [Wie].

I was unable to determine how much butyrate this would account for. I did find research comparing the SCFA levels produced in dogs under conditions of high fibre vs. This idea is supported by these observations:. Colonocyte butyrate metabolism was investigated in experimental colitis in mice. Colonocytes isolated from colitic and normal control mice were incubated with [ 14 C]butyrate or glucose, and production of 14 CO 2 , as well as of intermediate metabolites acetoacetate, beta-hydroxybutyrate and lactate , was measured.

The effect of different substrate concentrations on oxidation was also examined. Production of beta-hydroxybutyrate was decreased and production of lactate increased in DSS colitis compared with controls. Increasing butyrate concentration from 10 to 80 mM enhanced oxidation in DSS colitis 0. Surface and crypt epithelial cells showed similar ratios of butyrate to glucose oxidation. When 1 mM DSS was added to normal colonocytes in vitro, it did not alter butyrate oxidation.

The initial histological lesion of DSS administration was very patchy and involved crypt cells. Abnormal butyrate oxidation became apparent only after six days of DSS administration, at which time histological abnormalities were more widespread.

Histological abnormalities preceded measurable defects in butyrate oxidation. It was logical to assume that liver and muscle glycogen could serve as the fermentable substrate for lactate production in the stomach, but most of this should have been digested and absorbed by the small intes tine. Another possible source of ferment able substance which could survive passage through the small intestine is the protein- polysaccharides of the connective tissue ground substance found in abundance in the meat by-products and whole ground chicken.

The ground substance is made up of chondroitin sulfates and hyaluronic acid. The polysaccharide portion of these substances is composed of long chains of disaccharide units consisting of glucosa- mine or galactosamine and glucuronic acid.

The linkages of these polysaccharides are not such that they can be cleaved by the endogenous digestive enzymes found in the gut but they could be split by microbial enzymes. However, the ability and timing of SCFA to augment adaptation in the neonatal intestine is unknown. Furthermore, the specific SCFA inducing the intestinotrophic effects and underlying regulatory mechanism s are unclear.

Within each group, piglets were further randomized to examine acute 4, 12, or 24 hours and chronic 3 or 7 days adaptations. Indices of intestinal adaptation, including crypt-villus architecture, proliferation and apoptosis, and concentration of the intestinotrophic peptide, glucagon-like pepide-2 GLP-2 , were measured.

Indicative of an antiapoptotic profile, jejunal Bax: The intestinotrophic mechanism s underlying butyrate's effects may involve GLP Ultimately, butyrate administration may enable an infant with short-bowel syndrome to successfully transition to enteral feedings by maximizing their absorptive area. The question of whether or not to use probiotics continues to be debated.

It may be important to communicate to IBD patients that high-fiber foods are not recommended, especially for those with CD, during flares or in the presence of active disease states, fistulas or strictures. There appears to be a tendency among the dietary guidelines to restrict foods such as raw fruits, raw vegetables, beans, bran, popcorn, seeds, nuts, corn hulls, whole grains, brown rice and wild rice. Although not mentioned, raw salads would also fall into this category.

Few research studies are available to support or refute such a recommendation. The topic needs further investigation because patients with malabsorption may be at risk of not obtaining their necessary essential fatty acids. Perhaps saturated fats should be limited, with more of an emphasis on more healthy fat intakes.

The abundance of the AA-fermenting bacteria in the large intestine is very high and their number can reach up to per gram dry feces Smith and Macfarlane, Using the traditional plate counting technique, the authors have also reported that the dominant bacterial species for the utilization of single AA or pairs of AA are very different. For instance, Clostridium bifermentans is the predominant bacteria for the utilization of lysine or proline, and pairs of AA e.

Many species of bacteria utilize the same AA as substrates for growth Smith and Macfarlane, Overall, bacteria belonging to the Clostridium spp. The FOS and collagen showed comparable acetate production.

Collagen not only had a high production of total SCFA but also resulted in a greater acetate to propionate ratio relative to all other substrates 8.

Considerable variation in BCFA ratios was observed among substrates. So, knowledge on the mechanisms involved in its membrane transport is relevant to both its physiological and pharmacological benefits. Also, changes in transporter expression or function will have an obvious impact on the effect of BT, and therefore, knowledge on the regulation of its membrane transport seems particularly important. More specifically, BT is transported into normal colonic epithelial cells by both MCT1 and SMCT1, but its intracellular concentration is kept low because it is efficiently metabolized and effluxed from these cells by BCRP-mediated transport.

In these cells, BT accumulates intracellularly because it is inefficiently metabolized due to the fact that glucose becomes the primary energy source of these cells and because there is a reduction in BCRP expression. Butyrate is thought to exert its cellular effects through the induction of histone hyperacetylation. We sought to determine the effects of a variety of the SCFA on colon carcinoma cell growth, differentiation and apoptosis.

HT or HCT wild-type and pdeleted cells were treated with physiologically relevant concentrations of various SCFA, and histone acetylation state was assayed by acid-urea-triton-X gel electrophoresis and immunoblotting. Growth and apoptotic effects were studied by flow cytometry, and differentiation effects were assessed using transient transfections and Northern blotting. Propionate C3 and valerate C5 caused growth arrest and differentiation in human colon carcinoma cells.

The magnitude of their effects was associated with a lesser degree of histone hyperacetylation compared with butyrate. Acetate C2 and caproate C6 , in contrast, did not cause histone hyperacetylation and also had no appreciable effects on cell growth or differentiation.

Butyrate also significantly increased apoptosis, whereas the other SCFA studied did not. The growth arrest induced by the SCFA was characterized by an increase in the expression of the p21 cell-cycle inhibitor and down-regulation of cyclin B1 CB1.

These data suggest that the antiproliferative, apoptotic and differentiating properties of the various SCFA are linked to the degree of induced histone hyperacetylation. Furthermore, SCFA-mediated growth arrest in colon carcinoma cells requires the p21 gene.

Since butyrate is expected to impact cellular metabolic pathways in colon cancer cells, we hypothesize that it could exert its antiproliferative properties by altering cellular metabolism. We show that although Caco2 colon cancer cells oxidized both butyrate and glucose into CO2, they displayed a higher oxidation rate with butyrate as substrate than with glucose.

Furthermore, butyrate pretreatment led to an increase cell capacity to oxidize butyrate and a decreased capacity to oxidize glucose, suggesting that colon cancer cells, which are initially highly glycolytic, can switch to a butyrate utilizing phenotype, and preferentially oxidize butyrate instead of glucose as energy source to produce acetyl coA.

Butyrate pretreated cells displayed a modulation of glutamine metabolism characterized by an increased incorporation of carbons derived from glutamine into lipids and a reduced lactate production. The butyrate-stimulated glutamine utilization is linked to pyruvate dehydrogenase complex since dichloroacetate reverses this effect.

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