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Inside the Gut
Short Chain Fatty Acids (SCFAs)
Along with outcompeting the LPS producing bacteria that trigger inflammation, one of the primary and most basic ways by which probiotic bacteria work their magic is by fermenting prebiotics to produce SCFAs (primarily acetate, butyrate, and propionate). So, we are going to talk a bit about those, now.
SCFAs primarily work through three mechanisms:
1) Decreasing inflammation and permeability in the gut
2) Activation of free fatty acid receptors, FFAR2 and FFAR3, in the gut
3) Inhibition of Histone De-Acetylase (HDAC) in skeletal muscle
We will talk about the first one, now, as it occurs wholly inside the gut (though, it ultimately prevents bad things outside of it). The second one begins in the gut, but mostly does its work outside, so we will cover it a bit here, then get deeper into it and number 3, later, in the section on all of the stuff outside of the gut.
I should probably further emphasize that the Gut-Microbiota-Muscle axis is not straight-forward linear and compartmentalized. There is inside and out, as well as back and forth, communication. There are also overlapping functions and pathways. LPS/inflammation increases gut barrier breakdown, thus its own leakage into the body, and SCFAs/butyrate directly reduce inflammation in addition to reducing LPS/inflammatory leakage by strengthening barrier function… in addition to directly attacking problems caused by inflammation related pathways in skeletal muscle.
Anyway, back to SCFAs. Both acetate and propionate reduce inflammatory pathways of lipopolysaccharide like TNF-alpha and NF-kB (238, 239). However, butyrate is significantly more potent (240, 241). Butyrate also plays the most critical role in maintaining colonic health via modulation of intestinal cell growth and differentiation (242). It is the primary fuel source for enterocytes, being responsible for up to about 70% of their energy use (243, 244). Butyrate also dose-dependently reduces LPS impairment of tight junction permeability and intestinal barrier integrity.
We’ll get into this more in muscle, but one mechanism by which it increases tight junction proteins is by preventing LPS induced inhibition of the anabolic Akt/mTOR mediated protein synthetic pathway (245).
Butyrate also dose-dependently increases mucin protein contents of the mucosal layer of the intestine (246). The mucosal layer is the first line of defense against noxious substances and pathogens (247, 248). In addition to being food for some of the best bacteria, mucin improves adherence of probiotics to the mucosal layer of the intestine, thus mucins are perhaps the most important aspects of their viability and colonization (249, 250).
Butyrate also improves intestinal barrier function via activation of AMPK (251). Sodium butyrate has been specifically found to be an AMPK agonist (252). And, butyrate increase tight junction assembly, thus improving barrier function, specifically through AMPK (253, 254). This seems like as good of a place as any to add a bit more about AMPK, really quickly, as it is one of the major targets in all of this inside the gut.
AMPK is a primary signaler in the maintenance of tight junction integrity and intestinal barrier function. It is one of the most important pathways in preventing the “leaky gut” we have spoken of earlier in regard to LPS and other inflammatory and infectious molecules escaping into the body to wreak havoc (255, 256). As we’ve mentioned, modern food processing and the Western diet is a particularly egregious malefactor in all of this (257).
In addition to its involvement in barrier function, AMPK activation is extremely positive for the great bacteria that we can’t get commercially.
Metformin increased Akkermansia 18-fold through AMPK activation. Also, against a high-fat diet, it restored Bacteroides levels and normalized microbiota constituent ratios to that of lean subjects (258, 259, 260). It inhibited LPS induced inflammation and gut permeability increases, while improving glucose uptake and insulin sensitivity (259). Akkermansia increases are likely at least partially due to greatly elevated production of its favorite food, mucin, which is stimulated by AMPK. Its activation also reduces insulin resistance and adipose tissue inflammation in a high-fat diet (260).
Free Fatty Acid Receptors
Activation of FFAR2 by SCFAs suppresses insulin signaling in adipocytes, which inhibits fat accumulation in adipose tissue and promotes the metabolism of lipids and glucose in other tissues such as muscle (S2). Propionate and butyrate also both activate intestinal gluconeogenesis. Butyrate does so through AMPK, while propionate works through a gut-brain neural circuit involving FFAR3 (261). This glucose then triggers a signal to the brain which normalizes whole body glucose homeostasis (262).
In a fasting state, as much as 62% of infused propionate is converted to glucose in the intestine, accounting for 69% of total glucose production (263). This is especially applicable to lower carb diets. Basically, it makes your brain think you are plenty fed with carbs/glucose. When the brain thinks the body is well-fed, energy intensive protein synthesis is supported. It also reduces peripheral gluconeogenesis, sparing amino acids for use in muscle tissue, while improving insulin sensitivity via reduced output of glucose from the liver (262). Short chain fatty acids, especially butyrate, are also direct precursors for ketone formation, obviously handy for ketogenic diets (264, 265).
Activation of FFAR2/3 by SCFAs also stimulates the release of the incretin hormone, glucagon-like peptide-1 (GLP-1), enhancing anabolic and anti-catabolic insulin signaling pathways in muscle (266, 267). We will discuss this more, later.
Protein Absorption and Efficiency
The earliest studies on pro- and prebiotics were done to replace antibiotics for increasing digestion/feed efficiency in livestock. They result in the production of more meat (i.e. muscle mass), in general, and more meat per unit of food given. So, let’s take a look at the mechanisms on how this works, and how it will work for you.
As we have briefly discussed, probiotics and prebiotics, via short chain fatty acids, increase the proliferation of intestinal epithelial cells, as well as increasing villus height and crypt depth, expanding total surface area for nutrient absorption. Likewise, increases in the quantity and quality of goblet cells increases mucin, helping to maintain optimal health and function of the intestine. Ultimately, this increases total nutrient digestibility in the intestinal tract (268).
SCFAs, and other organic acids such as lactic acid (produced by lactobacillus, thus the name), reduce pH, increasing bioavailability of protein (269). They also enhance the release of digestive proteases, increasing absorption of small peptides and amino acids by enterocytes. (270). Only 80–90% of protein is actually digested and made available as amino acids in the small intestine, and we obviously want it on the high end (271). This inefficiency results in the entry of a good chunk of undigested protein into the large intestine, which we will discuss more in a moment.
Once proteins have been digested and absorbed, we get to yet another area where probiotics and prebiotics, via SCFA acids, are useful – namely, in protein sparing. The gut has one of the highest rates of cellular and protein turnover of any tissue in the body. If cellular needs are not met by diet and supplementation, skeletal muscle proteolysis results, with amino acids being funneled from the periphery to the gut (272The liver and the gut account for 20 to 35% of whole-body protein turnover and energy expenditure, and your big brain gets a crack at those before your muscles, as well (273). Up to 50% of dietary amino acids are oxidized in first pass in the gut, with anabolic BCAAs being amongst the most favored (274).
Some of this is inevitable, as these amino acids go toward protein structures in the intestines, such as digestive enzymes, mucins, and the physical makeup of the intestinal cells, themselves. But, they are also heavily used for fuel if their favorite food, SCFAs (especially butyrate), are not available (275, 276) . Dietary amino acids are preferred over glucose as intestinal metabolic fuel, and the systemic availability of dietary amino acids is ultimately one of the biggest determinants of the growth rate of lean body tissues such as muscle (277).
And, indeed, both probiotics and prebiotics have been shown to enhance the entry of dietary amino acids into systemic circulation. While the increase in digestion and absorption is modest at around 5%, plasma levels are increased by as much as 30% by the protein sparing effect of SCFAs (278, 279). Given the figure of 50% of amino acids being oxidized in first pass in non-pre/probiotic subjects, for a 200lb person on the standard 1g/lb of bodyweight protein intake, we are talking about the equivalent of an extra 30g of protein per day making it to systemic circulation to be available to your muscles!
And, there is more. As we mentioned above, 10-20% of protein is unabsorbed in the small intestine and moves on to the large intestine (with plant proteins being more poorly absorbed than animal ones), which leads us to nitrogen/amino acid recycling by the gut microbiota (280, 281). This recycling is not only of the undigested protein, but also amino acids which have entered the ammonia/urea cycle, generally after having been oxidized for fuel, particularly for the metabolic needs of skeletal muscle (282, 283). Glutamine and the BCAAs are favorites, here (284 , 285).
Nitrogen/amino acid salvage and recycling by the gut back into the body amino acid pool is quite substantial, being equal to approximately one-half of total dietary intake (286). The gut microbiota’s recycling of ammonia and urea back into amino acids, especially from glutamine, BCAAs, and EAAs has been found to be on the order of 300+mg/kg/day (287, 288). For our 200lb man, this would be another 27 grams of protein per day reclaimed by the healthy and efficient gut to go toward muscle building. Other studies have found in the 15-30g/day range, but this was with smaller people and smaller intakes than bodybuilding and fitness types (289).
Lactobacillus have the best research in this regard, though it is an area absolutely begging for more research (290, 291). This nitrogen recycling seems to be of particular importance in the overnight fasting period when food/protein is not being consumed (292). Basically, it helps you stay anabolic 24-7.
All in all, this is massive!! Pun intended. Between greater peripheral delivery of amino acids and nitrogen/AA recycling, we are talking as much as 60g of protein a day, for a 200lb person consuming the typical 1g/lb of bodyweight. This is 2 meals worth of extra protein available to promote muscle growth.
Finally, data in animals have shown direct correlations of microbial make-up with superior growth and feed efficiency. There is no such data on humans, as they are not grown for food, yet. Families and genera of butyrate producing genera and species including the aforementioned Bacteroides, Roseburia, and Faecalibacterium prausnitzii were all highly represented on the superior growth and feed efficiency side, as you might expect from what we have learned so far (293, 294, 295, 296, 297).
Part 4 on Tuesday, June 26th
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In the last episode of The CKD Files, Derf and Dan Jr. had just returned home from the gym following their two hour glycogen depletion workout and had subsequently commenced preparations for the ensuing carb-up.
Setting: Daytime in a living room
DERF: Typical musclehead, 240+ lbs, sub 6% bodyfat, head shaved to hide the consequences of years of 5-alpha reductase activity, rummages through a tackle box full of pills, vials, and syringes.
DAN JR: who couldn't grow on a gram of tren a day, sits, rolling a joint.
DERFDude, I'm low on gear.
DAN JR.Yeah, me too. We should go back by the gym and see BigWill after we smoke this.
He takes a puff and hands it to Derf, who does the same.
DERFI'm gonna need to eat first.
DAN JR.(annoyed)Did you take your shot already??
He nods, a bit woozy. Dan just shakes his head, grabsa syringe, and stands up.Derf passes out.Dan heads to the kitchen and returns with a bottle of glucose. He draws some into the syringe and injects it into one of the giant veins on Derf's arm.
He comes to.
DERFThanks, dude. Let's hit McDonald's.
DAN JR.(shakes his head)That's far too high in fat. Glycogen storage and amino acid uptake are optimal right now -- We need high Glycemic Index carbohydrates. A post workout drink of dextrose and whey is ideal.
DERFBullshit. I haven't had anything except whey and flaxfor the last two weeks. I want some food.
DAN JR.Fine. But, we're not eating McDonald's -- we'll go toan all you can eat place.
Dan takes out a syringe and injects himself in thethigh.
Derf nods. Dan pulls out another.
He injects it and pulls out another.
Setting: Daytime at all All-You-Can-Eat Restaurant
They walk into the restaurant, anxious to begin refilling of glycogen stores and raising leptin levels. There are a couple of people in line in front of them, so they step back.
They stand there for a moment, already impatient, when an OBESE WOMAN waddles up and cuts in front of them in line.
They give each other a "What the fuck?!" look, then stare at her back, in a rage fueled by low blood sugar, serotonin depletion, and supraphysiological androgen levels.
Did that chubby bitch just cut in front of us?
Does she think we're just standing here to greet people as they walk in the door?
She doesn't need to be getting seconds anyway.
How much do you think she weighs?
I'm thinking maybe as much as four bills. But it's pretty hard to tell when they get that big... I'd say she's definitely pushing at least three and somechange... You'd think they'd have some kind of width limit to eat at all-you-can-eatrestaurants. You know?
Like the height requirements for rollercoasters?
Yeah. They should have a sign when you first walk in the door with a guy holding his arms out that says:
Dan holds his arms out really wide.
"You must not be this wide to eat at this restaurant." -- 'Cause if you are, you damn sure don't need to be eating at an all-you-can-eat restaurant.
She needs some EC.
Fuck EC, she needs DNP and some meth.
Maybe she just has low leptin levels.
Yeah, and maybe she swallowed a guy who swallowed a fly, but I fucking seriously doubt it. It takes a concerted effort to get that fat. You don't go to sleep one night looking like a normal human being and wake up the next day with 54% bodyfat. That doesn't happen. It takes years of determination and willpower. To look like that, there can be no skipping meals, no going to bed hungry, no exercise. Shit, just walking from the couch to the kitchen must burn more than a hundred calories when you weigh that much... I bet she keeps a crate of Krispy Kremes, in her fucking living room, so she can grab a box whenever the urge should strike... Low leptin levels my ass. I guarantee you that bitch gets three tiers of food on her tray.
She's just got more to love, that's all.
Derf walks up closer to her back. He pretends to spank her.
Big is beautiful. Ain't it baby.
(shaking his head)
Fat is not beautiful unless you're a sick, deviant motherfucker with a fetish for that shit. It just isn't aesthetically pleasing.
The Obese Woman continues piling food on her tray.
I mean, granted, culture and normal personal preferences play a role incertain aspects of what is considered beautiful at different times. For example: Hairstyles and fashion change -- certain trends are hip for a while, but fiveyears later are atrocious -- the 1980's come to mind.
But some things are universally beautiful. And certain things are universally not beautiful in any way, shape, or form.
Things like Nicole Bass, and pimples, and warts, and melted flesh from third degree burns... And well-fed bitches like her.
You make a good argument.
Don't kid yourself, Derf. I'm not finished. I haven't yet begun to ridicule.
You know it's gotta be unsanitary. I mean, can you imagine what kind ofbacteria and yeast and STD's and shit are spawning and fermenting betweeneach and every fucking chub roll on that immense body?
It's a sick thought.
Of course, it is. And the other day I heard on Oprah something about "foodaholism". Like it's a fucking disease, like cancer. Like they can't help. Like it's not their fault.
I did read on MFW about a study linking obesity to a virus.
Well, then the CDC needs to come out here and quarantine this bitch.
If it was a virus, what do you think they'd call it.
There's already a name for what she has. It's called "gluttony".
The Obese Woman turns around with two trays full of food, each with plates piled one on top of the other like a pyramid.
DAN JR .
(as she walks by)
How now, brown cow.
She doesn't respond. Derf laughs, and they finally approach the windowto order their long-awaited food.
The following was a fictional skit. Any resemblance to actual people, be they from your local gym or alt.support.fat-acceptance, is purely coincidental.
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You ever go to take a shit and realize you are right in the middle of a marathon? You ever cross the finish line only to see a competitor drop dead of heat stroke or a heart attack? Have you ever just felt tired and run down, for days after an event or during peak levels of training -- or gotten a respiratory infection? Well, it is not because you didn’t drink enough Gatorade, or carb load, or get the right running shoes. It is because of trillions of shitty little bacteria in your gut pumping out inflammatory agents which attack testosterone production, increase toxic ammonia, and biochemically overheat your muscles and brain. Neobium™ Sport™ delivers an inexhaustible probiotic blend and friends that fortify your gut, reverses the pro-inflammatory milieu, increase mitochondrial density and function, and protects against the catabolic pathways that hinder recovery and health.
Run your shit, don’t let it run you.
Temperature (Austin). 2016 Apr 28;3(2):240-251. eCollection 2016 Apr-Jun. Heat stress, gastrointestinal permeability and interleukin-6 signaling - Implications for exercise performance and fatigue. Vargas N(1), Marino F(1). Exercise in heat stress exacerbates performance decrements compared to normothermic environments. It has been documented that the performance decrements are associated with reduced efferent drive from the central nervous system (CNS), however, specific factors that contribute to the decrements are not completely understood. During exertional heat stress, blood flow is preferentially distributed away from the intestinal area to supply the muscles and brain with oxygen. Consequently, the gastrointestinal barrier becomes increasingly permeable, resulting in the release of lipopolysaccharides (LPS, endotoxin) into the circulation. LPS leakage stimulates an acute-phase inflammatory response, including the release of interleukin (IL)-6 in response to an increasingly endotoxic environment. If LPS translocation is too great, heat shock, neurological dysfunction, or death may ensue. IL-6 acts initially in a pro-inflammatory manner during endotoxemia, but can attenuate the response through signaling the hypothalamic pituitary adrenal (HPA)-axis. Likewise, IL-6 is believed to be a thermoregulatory sensor in the gut during the febrile response, hence highlighting its role in periphery - to - brain communication. Recently, IL-6 has been implicated in signaling the CNS and influencing perceptions of fatigue and performance during exercise. Therefore, due to the cascade of events that occur during exertional heat stress, it is possible that the release of LPS and exacerbated response of IL-6 contributes to CNS modulation during exertional heat stress. The purpose of this review is to evaluate previous literature and discuss the potential role for IL-6 during exertional heat stress to modulate performance in favor of whole body preservation. DOI: 10.1080/23328940.2016.1179380 PMCID: PMC4964994 PMID: 27857954
Compr Physiol. 2011 Oct;1(4):1883-928. doi: 10.1002/cphy.c100082. Integrated physiological mechanisms of exercise performance, adaptation, and maladaptation to heat stress. Sawka MN(1), Leon LR, Montain SJ, Sonna LA. This article emphasizes significant recent advances regarding heat stress and its impact on exercise performance, adaptations, fluid electrolyte imbalances, and pathophysiology. During exercise-heat stress, the physiological burden of supporting high skin blood flow and high sweating rates can impose considerable cardiovascular strain and initiate a cascade of pathophysiological events leading to heat stroke. We examine the association between heat stress, particularly high skin temperature, on diminishing cardiovascular/aerobic reserves as well as increasing relative intensity and perceptual cues that degrade aerobic exercise performance. We discuss novel systemic (heat acclimation) and cellular (acquired thermal tolerance) adaptations that improve performance in hot and temperate environments and protect organs from heat stroke as well as other dissimilar stresses. We delineate how heat stroke evolves from gut underperfusion/ischemia causing endotoxin release or the release of mitochondrial DNA fragments in response to cell necrosis, to mediate a systemic inflammatory syndrome inducing coagulopathies, immune dysfunction, cytokine modulation, and multiorgan damage and failure. We discuss how an inflammatory response that induces simultaneous fever and/or prior exposure to a pathogen (e.g., viral infection) that deactivates molecular protective mechanisms interacts synergistically with the hyperthermia of exercise to perhaps explain heat stroke cases reported in low-risk populations performing routine activities. Importantly, we question the "traditional" notion that high core temperature is the critical mediator of exercise performance degradation and heat stroke. Published 2011. This article is a U.S. Government work and is in the public domain in the USA. DOI: 10.1002/cphy.c100082 PMID: 23733692 [Indexed for MEDLINE]
Tissue Barriers. 2015 May 29;3(3):e1039691. doi: 10.1080/21688370.2015.1039691. eCollection 2015 Jul-Sep. Microbiota and the control of blood-tissue barriers. Al-Asmakh M(1), Hedin L(2). The gastro-intestinal tract is an ecosystem containing trillions of commensal bacteria living in symbiosis with the host. These microbiota modulate a variety of our physiological processes, including production of vitamins, absorption of nutrients and development of the immune system. One of their major functions is to fortify the intestinal barrier, thereby helping to prevent pathogens and harmful substances from crossing into the general circulation. Recently, effects of these microbiota on other blood-tissue barriers have also been reported. Here, we review the evidence indicating that gut bacteria play a role in regulating the blood-brain and blood-testis barriers. The underlying mechanisms include control of the expression of tight junction proteins by fermentation products such as butyrate, which also influences the activity of histone deacetylase. DOI: 10.1080/21688370.2015.1039691 PMCID: PMC4574894 PMID: 26451344
Acta Physiol Hung. 2005;92(2):121-37. Testosterone and endurance exercise: development of the "exercise-hypogonadal male condition". Hackney AC(1), Moore AW, Brownlee KK. During the last 30 years a large number of research studies have been conducted examining reproductive endocrine dysfunction in exercising women. The number of similar studies examining men is still relatively small. Nevertheless, an increasing amount of research studies in men indicate endurance exercise training has significant effects upon the major male reproductive hormone, testosterone, and the hypothalamic-pituitary-testicular axis that regulates reproductive hormones. This review article addresses one reproductive endocrine dysfunction found in exercising men, what has been deemed the "exercise-hypogonadal male condition". Specifically, men with this condition exhibit basal (resting-state) free and total testosterone levels that are significantly and persistently reduced. The exact physiological mechanism inducing the reduction of testosterone is currently unclear, but is postulated to be a dysfunction (or perhaps a readjustment) within the hypothalamic-pituitary-testicular regulatory axis. The time course for the development of the "exercise-hypogonadal condition" or the threshold of exercise training necessary to induce the condition remains unresolved. The potential exists for these reduced testosterone levels within the exercise-hypogonadal male to disrupt and be detrimental to some anabolic or androgenic testosterone-dependent physiological processes. Unfortunately, extremely few research studies have addressed whether such processes are affected, and thus findings are inconclusive. Conversely, the alterations in testosterone levels brought about by endurance exercise training have the potential for cardiovascular protective effects and thus could be beneficial to the health of these men. Current evidence suggests this condition is limited to men who have been persistently involved in chronic endurance exercise training for extended periods of time (i.e., years). Many questions, however, regarding the male reproductive endocrine adaptive process to exercise and exercise training remain unanswered, necessitating the need for further research on this topic. DOI: 10.1556/APhysiol.92.2005.2.3 PMID: 16268050 [Indexed for MEDLINE]
Eur J Appl Physiol. 2004 Apr;91(4):382-91. Epub 2003 Nov 8. New aspects of the hormone and cytokine response to training. Steinacker JM(1), Lormes W, Reissnecker S, Liu Y. Exercise training is associated with peripheral-cellular and central-cerebral processes, hormonal-neuronal regulation and transmission mechanisms. During the acute training response, peripheral cellular mechanisms are mainly metabolostatic to achieve energy supply and involve associated cytokine and hormonal reactions. Glycogen deficiency is associated with increased expression of local cytokines (interleukin-6, IL-6), decreased expression of glucose transporters, increased cortisol and decreased insulin secretion and beta-adrenergic stimulation. A nutrient-sensing signal of adipose tissue may be represented by leptin which, as for insulin, IL-6 and insulin-like growth-factor I (IGF-I), has profound effects on the hypothalamus and is involved in the metabolic hormonal regulation of exercise and training. Muscle damage and repair processes may involve the expression of inflammatory cytokines (e.g. tumour necrosis factor-alpha, TNF-alpha) and of stress proteins (e.g. heat shock protein 72). During overreaching and overtraining, a myopathy-like state is observed in skeletal muscle with depressed turnover of contractile proteins (e.g. in fast-type glycolytic fibres with a concomitant increase in slow type myosins). These alterations are influenced by exercise-induced hypercortisolism, and by decreased somatotropic hormones (e.g. IGF-I). The hypothalamus integrates various error signals (metabolic, hormonal, sensory afferents and central stimuli) and therefore pituitary releasing hormones represent the functional status of an athlete and long-term hypothalamic hormonal and sympathoadrenal downregulation are some of the prominent hormonal signs of prolonged overtraining and performance incompetence syndrome. DOI: 10.1007/s00421-003-0960-x PMID: 14608461 [Indexed for MEDLINE]
Br J Nutr. 2011 Jun 28;105(12):1729-33. doi: 10.1017/S000711451000557X. Epub 2011 Feb 16. Keto analogue and amino acid supplementation affects the ammonaemia response during exercise under ketogenic conditions. Prado ES(1), de Rezende Neto JM(2), de Almeida RD(1), Dória de Melo MG(3), Cameron LC(1). Hyperammonaemia is related to both central and peripheral fatigue during exercise. Hyperammonaemia in response to exercise can be reduced through supplementation with either amino acids or combined keto analogues and amino acids (KAAA). In the present study, we determined the effect of short-term KAAA supplementation on ammonia production in subjects eating a low-carbohydrate diet who exercise. A total of thirteen male cyclists eating a ketogenic diet for 3 d were divided into two groups receiving either KAAA (KEx) or lactose (control group; LEx) supplements. Athletes cycled indoors for 2 h, and blood samples were obtained at rest, during exercise and over the course of 1 h during the recovery period. Exercise-induced ammonaemia increased to a maximum of 35 % in the control group, but no significant increase was observed in the supplemented group. Both groups had a significant increase (approximately 35 %) in uraemia in response to exercise. The resting urate levels of the two groups were equivalent and remained statistically unchanged in the KEx group after 90 min of exercise; an earlier increase was observed in the LEx group. Glucose levels did not change, either during the trial time or between the groups. An increase in lactate levels was observed during the first 30 min of exercise in both groups, but there was no difference between the groups. The present results suggest that the acute use of KAAA diminishes exercise-induced hyperammonaemia. DOI: 10.1017/S000711451000557X PMID: 21324213 [Indexed for MEDLINE]
J Clin Gastroenterol. 2017 Apr;51(4):312-323. doi: 10.1097/MCG.0000000000000789. The Effects of Probiotics and Symbiotics on Risk Factors for Hepatic Encephalopathy: A Systematic Review. Viramontes Hörner D(1), Avery A, Stow R. Alterations in the levels of intestinal microbiota, endotoxemia, and inflammation are novel areas of interest in the pathogenesis of hepatic encephalopathy (HE). Probiotics and symbiotics are a promising treatment option for HE due to possible beneficial effects in modulating gut microflora and might be better tolerated and more cost-effective than the traditional treatment with lactulose, rifaximin or L-ornithine-L-aspartate. A systematic search of the electronic databases PubMed, ISI Web of Science, EMBASE, and Cochrane Library was conducted for randomized controlled clinical trials in adult patients with cirrhosis, evaluating the effect of probiotics and symbiotics in changes on intestinal microflora, reduction of endotoxemia, inflammation, and ammonia, reversal of minimal hepatic encephalopathy (MHE), prevention of overt hepatic encephalopathy (OHE), and improvement of quality of life. Nineteen trials met the inclusion criteria. Probiotics and symbiotics increased beneficial microflora and decreased pathogenic bacteria and endotoxemia compared with placebo/no treatment, but no effect was observed on inflammation. Probiotics significantly reversed MHE [risk ratio, 1.53; 95% confidence interval (CI): 1.14, 2.05; P=0.005] and reduced OHE development (risk ratio, 0.62; 95% CI: 0.48, 0.80; P=0.0002) compared with placebo/no treatment. Symbiotics significantly decreased ammonia levels compared with placebo (15.24; 95% CI: -26.01, -4.47; P=0.006). Probiotics did not show any additional benefit on reversal of MHE and prevention of OHE development when compared with lactulose, rifaximin, and L-ornithine-L-aspartate. Only 5 trials considered tolerance with minimal side effects reported. Although further research is warranted, probiotics and symbiotics should be considered as an alternative therapy for the treatment and management of HE given the results reported in this systematic review. DOI: 10.1097/MCG.0000000000000789 PMID: 28059938 [Indexed for MEDLINE]
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