Glutenlightgrani con glutine leggero e tollerabile
Header Image - Gluten Light
Gluten LightMagazine & Library

Tag Archives

3 Articles

A recent and in-depth research regarding the influence of gut microbiota, diet and exercise on intestinal permeability II part

by luciano

Link I part A recent and in-depth research regarding the influence of gut microbiota, diet and exercise on intestinal permeability. I Part

6 Exercise as a regulator of intestinal barrier integrity

Regular moderate physical exercises are one of the most common recommendations for the prevention of various pathologies, including disruption of the integrity of the intestinal barrier. This may be due to the influence of the gut microbiota. In particular, exercises have been found to increase gut bacterial diversity (Hintikka et al., 2023). However, effects of physical exercises depend on their intensity. For example, endurance athletes have a high incidence of gastrointestinal disorders and the “leaky” gut is one of the most common disorders (Ribeiro et al., 2021). It is characterized by dysfunction of the intestinal epithelial barrier and its excessive permeability. This results in penetration of harmful microorganisms, toxins or undigested food particles into the bloodstream and has a negative effect on health of the whole organism (Aleman et al., 2023).
The effect of exercise on intestinal permeability depends on its duration and intensity. For example, people who exercise frequently and intensely have the same mortality rates as people who lead a sedentary lifestyle (Van Houten et al., 2015). A 60 min bout of intensive treadmill running increased the permeability of the small intestine in runners, whereas low-intensity running had no such effect (Pals et al., 1997). Using the overtraining model with male C57BL/6 mice, it was established that exhaustive exercise exacerbated intestinal inflammation, disrupted integrity and enhanced intestine wall permeability (Hou et al., 2020). Sustained strenuous exercise in racing sled dogs increased the intestinal permeability and the frequency of gastric erosions or ulcerations (Davis et al., 2005). High-intensity interval running increased intestine wall permeability and intestinal-fatty acid binding protein (I-FABP) release in male runners (Pugh et al., 2017). I-FABP is a cytoplasmic protein expressed exclusively in the enterocytes of the small intestine and its increased concentration in the blood is used as a marker of damage to intestinal epithelial cells (Sikora et al., 2019).
Physical exercise of low/moderate intensity can often have positive effects and can be considered as a method of non-pharmacological intervention in inflammatory bowel disease (Ordille and Phadtare, 2023). For example, mice that swam for 30 min before inducing intestinal barrier dysfunction had less intestinal dysfunction compared to mice that had not swum before. This might happen due to a strengthening of antimicrobial function of the intestine as a result of the increase in expression of antimicrobial peptides (Luo et al., 2014). Obese mice that were trained on a motorized treadmill for 45 min per day 5 days a week for 12 weeks had higher expression levels of colonic ZO-1 and occludin. Moderate exercise effectively prevented the development of dysbacteriosis caused by the HFD, as well as intestinal pathology (Wang et al., 2022). Dysbacteriosis and impaired intestinal barrier integrity induced by HFD in wild type mice was prevented by exercise. Exercise on a motor-driven rodent treadmill for 5 days a week for a total of 15 weeks significantly reversed the pathological changes. Ablation of Sestrin 2 protein attenuated the protective effects of exercise, suggesting its involvement in regulation of intestinal permeability (Yu et al., 2022). Thus, it can be concluded that high-intensity exercises often have a negative effect on the integrity of the intestine, whereas low- and moderate-intensity regular exercise can have a positive effects. It may be speculated that moderate damage to the intestinal wall is a hormetic factor that may be used to train organisms to cope with severe damaging challenges. This may be used to increase the adaptive potential of organisms to prevent damaging effects of any stresses of physical and chemical nature on the integrity of the intestinal wall.

6.1 Exercise-induced heat stress

It is known that physical exertion causes heat stress and associated dysfunction of gut integrity. A systematic review examining the relationship between an exercise-induced increase in core body temperature and intestinal permeability demonstrated that the magnitude of exercise-induced hyperthermia correlated with increased intestinal permeability (Pires et al., 2017). An increase in body temperature is a signal to activate the expression of heat shock proteins (HSP) which constitutively function as molecular chaperones maintaining the native structure of the proteins. Their expression is mainly triggered by heat shock signals. During exercise, the level of HSP70 and HSP90 increase (Krüger et al., 2019). Expression of HSP is regulated at the level of heat shock factors (HSF) such as HSF1 that is expressed in all mammalian tissues. Normally it resides in the cytoplasm as a monomer. In response to stressful conditions, it trimerizes, translocates into the nucleus, binds to the heat shock element of target genes and activates the transcription of HSPs, including HSP70/90 (Noble and Shen, 2012).
In this way, exercises cause a homeostatic imbalance, while regular training is adaptive and decreases the degree of this imbalance. Potentially, a higher adaptive steady-state level of HSPs due to regular training could explain their positive effect on gut integrity. At that time, during acute physical exertion, HSPs probably cannot cope with that level of homeostatic imbalance caused exercise-induced heat stress.

6.2 Exercise-induced hypoxia
It is well known, that exercise causes a redistribution of blood flow between tissues. This leads to the development of hypoxia (decreased oxygen levels) in intestinal epithelial cells and activation of hypoxia-inducible factor alpha (HIF-1α) (Wu et al., 2020). Figure 3 schematically shows the influence of exercise-induced hypoxia on intestinal permeability. In normoxia (normal oxygen levels), prolyl hydroxylase hydroxylates HIF-1α at two proline residues (Pro 402 and Pro 564). This results in ubiquitination followed by subsequent proteasomal degradation of HIF-1α (Lee et al., 2004).

intestinal barrier

…..omissis

7 Conclusion and perspectives
The intestinal wall is a kind of checkpoint between the external and internal environments of organisms. The wall consists of three layers: mucous, epithelial, and lamina propria. The mucous layer is inhabited by microorganisms, many of which mutually beneficially coexistence within the human body. These microorganisms modulate many if not most living processes: from the development of the immune and nervous systems at early stages of life to the induction of chronic inflammation causing neurodegeneration at aging. Despite the fact that these microorganisms have coexisted with humans for many years, under certain conditions the enteral immune system of the lamina propria can perceive them as foreign and trigger a pro- inflammatory response.
Normally, the intestinal mucosa is semipermeable. It allows selective absorption of nutrients into the bloodstream but prevents the entrance of potentially harmful microorganisms and their waste products from contact with the enteral immune system. An imbalance of the intestinal microbiota, called dysbiosis, can cause a disturbance of intestinal integrity and increase intestinal permeability. Conversely, a healthy composition of the gut microbiota can contribute to the integrity of the intestinal barrier due to increased expression and induction of the assembly of TJ proteins, activation of mucus synthesis, and antioxidant action.
Disruption of intestinal barrier function may trigger development of local and even systemic inflammation.
…..omissis
In general, a vicious cycle of intestinal barrier disruption can be traced here, as excessive intestinal wall permeability provokes the development of chronic low-grade inflammation. The latter is characterized by increased production of pro-inflammatory cytokines and enhanced ROS generation, increasing intestinal barrier dysfunction.
Nutrition looks to be the simplest non-pharmacological effector of integrity and permeability of the intestinal wall. It can have both a negative effect, such as HFD inducing metabolic endotoxemia, or a positive effect, such as a diet rich in plant polyphenols or fermented dairy products, increasing the expression of TJ proteins and promoting the development of beneficial bacteria.
Exercise also can affect gut intestinal permeability. Its effects depend on duration and intensity of exercise. Acute extensive physical exertion often increases intestinal permeability which may be related to the induction of heat stress, that organisms cannot cope with at that time due to insufficient resources. On the other hand, regular low and moderate intensity exercises, that are adaptive in nature, mostly have a positive effect on the integrity of the intestine and decrease its permeability. Potentially, this may be associated with an increase in the steady-state level of HSPs and chronic activation of HIF-1α which activates the transcription of genes responsible for strengthening the intestinal barrier function.
In general, it can be concluded that proper nutrition which promotes a healthy biodiversity of the gut microbiota, combined with moderate exercise, contribute to the integrity of the intestine. Disbalanced nutrition and excessive physical activity can provoke the development of dysbacteriosis and increase intestinal permeability which can potentially lead to a pro-inflammatory response. Figure 4 schematically shows potential consequences of acute intense exercises, unhealthy diet (e.g., high-fat diet), and dysbiosis on the intestinal barrier.
Taking into account all of the above, we can outline the following future prospects:
1. Development of healthy diets to support intestinal homeostasis;
2. Use of fermented dairy products as natural pre-, pro- and postbiotics to promote a healthy gut;
3. Selection of exercises to promote intestinal integrity by frequency, intensity and duration;
4. Study of the role of intestinal HIF-2α during exercise;
5. Systemic investigation of hypoxia-induced oxidative stress as a regulator of intestinal wall permeability.
Most of these perspective avenues are directed to enhance the capability of organisms to cope with disturbing factors. That increases an adaptive capability via preadaptation/hormetic mechanisms. However, some of them may be used “to patch holes” in “leaky” intestinal wall, which is characterized by increased specific permeability of the intestinal epithelium. Intestinal barrier permeability: the infuence of gut microbiota, nutrition, and exercise. Tetiana R. Dmytriv et al. DOI 10.3389/fphys.2024.1380713. PUBLISHED 08 July 2024

Note
[1] The term “intestinal barrier” emphasizes the barrier function of the intestinal wall which protects organism against invading by bacteria or other microorganisms and potentially toxic components of microorganisms. In fact, it is a complex selective physical barrier that separates the internal environment of the body from the contents of the intestinal lumen (Bischoff et al., 2014). Figure 1 shows a schematic structure of the intestinal barrier. It consists of several layers: i) a mucous layer including inner and outer mucous sublayers inhabited by commensal microorganisms in a different extent, ii) a single layer of epithelial cells, and iii) the lamina propria, which consists of immune cells that instantly react to the invasion of foreign substances (Schoultz and Keita, 2020).
The first layer, the mucous layer, that consists mainly of a mesh polymer called mucin, is located on the side of the intestinal lumen. It is associated with community of commensal microorganisms, including bacteria, fungi, viruses, and parasites, that form the individual microbial community (Chelakkot et al., 2018). A change in the microbial composition that causes a sharp imbalance between beneficial and potentially pathogenic bacteria, including changes in its functional composition, metabolic activity or changes in their local distribution, is called dysbiosis or dysbacteriosis. The latter usually results from loss of beneficial bacteria, overgrowth of potentially pathogenic bacteria, or loss of overall bacterial diversity. This disrupts the homeostatic balance of the intestinal microbiota and has a negative impact on the host’s health. In particular, dysbacteriosis is implicated in a wide range of diseases (DeGruttola et al., 2016).
The second layer, the intestinal epithelium, consists of a single layer of several specialized epithelial cells, such as enterocytes, Goblet cells, Paneth cells, enteroendocrine cells, and microfold cells (Figure 1). Enterocytes form the basis of the intestinal epithelium and play a main role in the absorption of all consumed nutrients. Goblet cells constitute about 10% of specialized epithelial cells. They secrete mucus to protect the intestinal wall from digestive enzymes (Kim and Ho, 2010). Paneth cells contain secretory granules filled with antimicrobial peptides, that are secreted in low amounts constitutively and provide the antimicrobial properties of the intestinal mucosa. Under certain conditions, their secretion can increase dramatically (Yokoi et al., 2019). Enteroendocrine cells produce hormones regulating secretion of digestive enzymes and insulin, peristalsis of the intestine, satiety, and immune response (Bonis et al., 2021). Microfold cells transport bacteria and antigens from the epithelium to enteric immune cells that either activate or suppress the immune response (Jung et al., 2010). All these cell types collectively contribute significantly to gut homeostasis.
The third layer, lamina propria, is located under the epithelium and forms the enteric immune system that consists of a large number of leukocytes with macrophages and dendritic cells being the dominant cell types (Shemtov et al., 2023). Resident intestinal macrophages are located in close proximity to the gut microbiota, with which they often interact. They play a key role in immune sampling of luminal bacteria, contributing to the maintenance of intestinal homeostasis and regulated immune response.

[2] TJ proteins are a complex of transmembrane and cytoplasmic proteins that form tight junctions, which seal cells together to create a selective barrier, maintain cell polarity, and regulate cell processes.

Key words
tight junction, tight junction proteins, inflammation,

Gluten-Free Diet

by luciano

Highlight

-Omissis…….GFD implied a reduction in bacterial populations generally regarded as beneficial for human health such as Bifidobacterium and Lactobacillus, and an increase in those of opportunistic pathogens such as Escherichia coli and total Enterobacteriaceae.
-Omissis…Hansen et al. showed that minimal amounts of gluten are sufficient to affect the microbiota population, lowering the Bifidobacteria count in patients adhering to a low-gluten regimen.
-Omissis…Some changes in the abundance of 8 families of bacteria were observed during the GFD period: Veillonellaceae, Ruminococcus bromii and Roseburia faecis, decreased, whereas Victivallaceae, Clostridiaceae, ML615J-28, Slackia and Coriobacteriaceae increased during GFD. Veillonellaceae, a pro-inflammatory family of Gram-negative bacteria known for lactate fermentation, increase in diseases such as IBD, irritable bowel syndrome and liver cirrhosis.
-Omissis.…This review appraised the current knowledge about the gut microbiota in health as well as CD and NCG/WS and the related effects evoked by GFD in these two most common conditions. The evidence so far acquired has demonstrated that diseases are often characterized by an imbalance in the microbial intestinal population composition, leading to dysbiosis, a condition promoting inflammation and metabolic impairment.

Research reviewed

1 – Effects of a gluten-free diet on gut microbiota and immune function in healthy adult human subjects. Published online by Cambridge University Press: 18 May 2009. Giada De Palma , Inmaculada Nadal , Maria Carmen Collado and Yolanda Sanz
…omissis. “Therefore, introduction of a GFD implied a reduction in bacterial populations generally regarded as beneficial for human health such as Bifidobacterium and Lactobacillus, and an increase in those of opportunistic pathogens such as Escherichia coli and total Enterobacteriaceae. These changes could be related to reductions in polysaccharide intake, since these dietary compounds usually reach the distal part of the colon partially undigested, and constitute one of the main energy sources for beneficial components of the gut microbiota(Reference De Graaf and Venema27). In addition, reductions in Bifidobacterium and Lactobacillus populations relative to Gram-negative bacteria (Bacteroides and Escherichia coli) were previously detected in untreated CD children and particularly in treated CD patients with a GFD(Reference Nadal, Donat and Ribes-Koninckx7). These findings indicate that this dietary therapy may contribute to reduce beneficial bacterial group counts and increase enterobacterial counts, which are microbial features associated with the active phase of CD(Reference Nadal, Donat and Ribes-Koninckx7, Reference Collado, Donat and Ribes-Koninckx28) and, therefore, it would not favour completely the normalisation of the gut ecosystem in treated CD patients”.

2 – Effect of Gluten-Free Diet on Gut Microbiota Composition in Patients with Celiac Disease and Non-Celiac Gluten/Wheat Sensitivity. Giacomo Caio, Lisa Lungaro, Nicola Segata, Matteo Guarino, Giorgio Zoli, Umberto Volta, and Roberto De Giorgio. Nutrients. 2020 Jun; 12(6): 1832. Published online 2020 Jun 19. doi:10.3390/nu12061832

“Celiac disease (CD) and non-celiac gluten/wheat sensitivity (NCG/WS) are the two most frequent conditions belonging to gluten-related disorders (GRDs). Both these diseases are triggered and worsened by gluten proteins ingestion, although other components, such as amylase/trypsin inhibitors (ATI) and fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs), seem to be involved in the NCG/WS onset. Therefore, the only effective treatment to date is the long-life adherence to a strictly gluten-free diet. Recently, increasing attention has been paid to the intestinal barrier, a dynamic system comprising various components, which regulate the delicate crosstalk between metabolic, motor, neuroendocrine and immunological functions. Among the elements characterizing the intestinal barrier, the microbiota plays a key role, modulating the gut integrity maintenance, the immune response and the inflammation process, linked to the CD and NCG/WS outbreak. This narrative review addresses the most recent findings on the gut microbiota modulation induced by the gluten-free diet (GFD) in healthy, CD and NCG/WS patients”.
Omissis…..7. Gluten-Free Diet Effects on Healthy Human Microbiota.
The overall literature search on databases including the terms “gluten free diet”, “GFD”, “gluten free diet AND healthy”, “microbiota”, “microbiome”, “microbiome AND healthy patients”, “microbiota AND healthy patients” produced 2775 results. Of these, excluding duplicates, three fulfilled our inclusion criteria. In 2009, De Palma et al. [101] explored whether a month of GFD affects the microbiota composition of ten healthy subjects. Enumeration of fecal bacteria by fluorescence in situ hybridization (FISH) using 16S rRNA-targeted oligonucleotide probes showed that GFD causes a decrease in the count of Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii. Quantitative PCR (qPCR) characterization of fecal microbes following GFD revealed a reduction in the number of Bifidobacterium, Lactobacillus and Bifidobacterium longum and an increase in the Enterobacteriaceae and Escherichia coli counts. They propose that the depletion in Bifidobacterium and Lactobacillus, generally considered as probiotics, could be caused by the reduced availability of polysaccharides introduced with the GFD that serve as a substrate for gut microbiota. Moreover, the reduction in Faecalibacterium prausnitzii, along with the concomitant increase in the opportunistic pathogens Enterobacteriaceae and Escherichia coli in the fecal mucus of active Crohn’s disease patients was found to trigger the inflammatory insult [89,102,103]. Moreover, Hansen et al. showed that minimal amounts of gluten are sufficient to affect the microbiota population, lowering the Bifidobacteria count in patients adhering to a low-gluten regimen [104]. Indeed, the authors performed a randomized, controlled, cross-over trial study involving 60 non-CD Danish adults who followed a low-gluten diet (2 g gluten per day) for eight weeks and then switched to a high-gluten diet (18 g gluten per day) for another eight weeks, including a washout period of at least six weeks of normal diet (12 g gluten per day) between the two diets. Notably, GFD was associated with an increase of unclassified species of Clostridiales and an unclassified species of Lachnospiraceae, whereas E. hallii and A. hadrus (both butyrate-producers), Dorea (hydrogen producer) and the hydrogen-consumer and acetate-producer Blautia, in addition to two species of the Lachnospiraceae and four species of Bifidobacterium, were found to decrease. These microbial changes could be ascribed to the low-gluten diet availability of arabinoxylan and arabinoxylan-oligosaccharides, as these food components are abundant non-starch polysaccharides of cereal grains, which serve as energy substrates for the bacterial species mentioned above [105,106,107,108,109,110]. Bonder et al. [111] investigated the gut microbiota of 21 healthy volunteers on a GFD for four weeks, tested with a total of 9 stool samples for each person (one at baseline, four during the GFD and four when they returned to their usual diet). The microbiome profile was then characterized using 16 sRNA sequencing and investigated for taxonomic and implied functional compositions. Overall, the bacterial profile remained relatively stable in healthy individuals on GFD. However, some changes in the abundance of 8 families of bacteria were observed during the GFD period: Veillonellaceae, Ruminococcus bromii and Roseburia faecis, decreased, whereas Victivallaceae, Clostridiaceae, ML615J-28, Slackia and Coriobacteriaceae increased during GFD. Veillonellaceae, a pro-inflammatory family of Gram-negative bacteria known for lactate fermentation, increase in diseases such as IBD, irritable bowel syndrome and liver cirrhosis [88,112,113], while they decrease in autistic patients [114]. Compared to a normal diet, the abundance of Ruminococcus bromii, known to degrade the resistant starch in the human colon [115] and the cellulose, producing short chain fatty acids (SCFA) and hydrogen gas [116], was affected by the different starch composition of GFD. Coriobacteriaceae (Slackia genus in particular) and Clostridiaceae were associated with CD, IBD and colorectal cancer [117,118,119]. Thus, gluten withdrawal alters mostly bacterial species, utilizing carbohydrate and starch as energy substrates. The effects of GFD on the abundance of bacterial populations in healthy patients are illustrated in Figure 1.

……omissis. Growing evidence indicates that the interplay between gut microbiota and intestinal epithelial barrier function play a critical role in priming and maintaining a competent immune system. All together, these factors generate a gastrointestinal ecosystem, which, in concert with the classic repertoire of gut physiology, prevent the detrimental effect of various noxae. Offending foods belongs to those harmful substances able to perturb the gastrointestinal ecosystem, thereby leading to disease states. In this wide research area that is still far from being clarified, even classic dietary factors, such as wheat and related gluten and amylase trypsin inhibitors, can play a role in symptom generation in genetically susceptible or sensitive patients. This review appraised the current knowledge about the gut microbiota in health as well as CD and NCG/WS and the related effects evoked by GFD in these two most common conditions. The evidence so far acquired has demonstrated that diseases are often characterized by an imbalance in the microbial intestinal population composition, leading to dysbiosis, a condition promoting inflammation and metabolic impairment. In CD, the depletion of probiotic species, i.e., Lactobacillus and Bifidobacteria and the relative increase of pro-inflammatory bacteria, e.g., Veillonaceae genus, represent microbiota fingerprints likely contributing to disease onset, which is common to CD patients. In all the groups analyzed, GFD was shown to reduce bacterial richness while affecting gut microbiota composition in a different manner depending on health (asymptomatic subjects) and disease state (CD and NCG/WS). Indeed, in healthy subjects, GFD causes the depletion of beneficial species, e.g., Bifidobacteria, in favour of opportunistic pathogens, e.g., Enterobacteriaceae and Escherichia coli. Conversely, in CD and NCG/WS, GFD evoked a positive effect on gastrointestinal symptoms by helping to restore the microbiota population and by lowering pro-inflammatory species. In conclusion, these studies shed light on the complex interactions occurring between diet, gut barrier and gut microbiota. Multiple aspects are still to be explored along the microbiome-diet axis, including investigations into the yet-to-be-defined species that constitute large fractions of the microbiome [84], as well as the role of strain-specific microbial determinants and the difficulties in capturing detailed dietary information in large diverse metagenomics cohorts. In addition to general investigations of the complex link between diet, microbiome and health, further studies are particularly needed to specifically improve our knowledge of the effects that GFD could exert on the bacterial species involved within CD and NCG/WS”.

3 – The influence of a short-term gluten-free diet on the human gut microbiome. Marc Jan Bonder et al. Genome Medicine (2016)

“Abstract.

Background: A gluten-free diet (GFD) is the most commonly adopted special diet worldwide. It is an effective treatment for coeliac disease and is also often followed by individuals to alleviate gastrointestinal complaints. It is known there is an important link between diet and the gut microbiome, but it is largely unknown how a switch to a GFD affects the human gut microbiome.

Methods: We studied changes in the gut microbiomes of 21 healthy volunteers who followed a GFD for four weeks. We collected nine stool samples from each participant: one at baseline, four during the GFD period, and four when they returned to their habitual diet (HD), making a total of 189 samples. We determined microbiome profiles using 16S rRNA sequencing and then processed the samples for taxonomic and imputed functional composition. Additionally, in all 189 samples, six gut health-related biomarkers were measured.

Results: Inter-individual variation in the gut microbiota remained stable during this short-term GFD intervention. A number of taxon-specific differences were seen during the GFD: the most striking shift was seen for the family Veillonellaceae (class Clostridia), which was significantly reduced during the intervention (p = 2.81 × 10−05 ). Seven other taxa also showed significant changes; the majority of them are known to play a role in starch metabolism. We saw stronger differences in pathway activities: 21 predicted pathway activity scores showed significant association to the change in diet. We observed strong relations between the predicted activity of pathways and biomarker measurements.

Conclusions: A GFD changes the gut microbiome composition and alters the activity of microbial pathways”.

Key words: gut, microbiota, Free-Diet, Lactobacillus, Bifidobacteria, pro-inflammatory bacteria, opportunistic pathogens, Enterobacteriaceae, Escherichia coli

Einkorn Wheat and Intestinal Microbiota

by luciano

The state and health of the intestinal microbiota is at the center of many studies aimed at studying the role of the microbiota in diseases and how to intervene for preventive or curative purposes.
The set of microorganisms that populate our digestive system (microbiota) includes good bacterial strains but harmful ones can sometimes also be present. Indigenous strains (those that characterize our microbiota) hinder the colonization of the intestine by new microbes, including pathogenic ones. Vitamin K, for example, is synthesized by good bacteria present. Indigenous bacteria digest and ferment the favonoids contained in fruits and vegetables, promoting the production of substances that have protective effects on cardiovascular health. An essential function that our bacteria perform is to produce short-chain fatty acids, especially butyric acid. These acids protect the intestine from inflammation and the onset of tumors.
La ricerca “In Vivo Effects of Einkorn Wheat (Triticum monococcum) Bread on the Intestinal Microbiota, Metabolome, and on the Glycemic and Insulinemic Response in the Pig Model” ha questo tema come focus.
Highlighted:
Abstract: “Einkorn wheat (Triticum monococcum) is characterized by high content of proteins, bioactive compounds, such as polyunsaturated fatty acids, fructans, tocols, carotenoids, alkylresorcinols, and phytosterols, and lower α-, β -amylase and lipoxygenase activities compared to polyploid wheat. These features make einkorn flour a good candidate to provide healthier foods. In the present study, we investigated the effects of einkorn bread (EB) on the intestinal physiology and metabolism of the pig model by characterizing the glycemic and insulinemic response, and the microbiota and metabolome profiles. Sixteen commercial hybrid pigs were enrolled in the study; four pigs were used to characterize postprandial glycemic and insulinemic responses and twelve pigs underwent a 30-day dietary intervention to assess microbiota and metabolome changes after EB or standard wheat bread (WB) consumption. The postprandial insulin rise after an EB meal was characterized by a lower absolute level, and, as also observed for glucose, by a biphasic shape in contrast to that in response to a WB meal. The consumption of EB led to enrichment in short-chain fatty acid producers (e.g., Blautia, Faecalibacterium, and Oscillospira) in the gut microbiota and to higher metabolic diversity with lower content of succinate, probably related to improved absorption and therefore promoting intestinal gluconeogenesis. The observed changes, at both a compositional and metabolic scale, strongly suggest that EB consumption may support a health-promoting configuration of the intestinal ecosystem.”

omissis……

“Einkorn wheat (Triticum monococcum) was one of the first crops domesticated approximately 12,000 years ago in the Near East, alongside emmer wheat (Triticum dicoccum). Typically, einkorn was cultivated on marginal agricultural land, being able to survive in harsh environments and poor soils where other types of wheat could not survive. Spelt wheat (Triticum spelta) represents a hexaploid series of the Triticum genome constitution, which is characterized by great adaptation to a wider range of environments [1]. When compared to polyploid wheats, it has a higher content of proteins and some well recognised bioactive compounds, such as polyunsaturated fatty acids, fructans, tocols, carotenoids, alkylresorcinols, phytosterols, and lower α-, β -amylase and lipoxygenase activities [2]. These compositional traits make einkorn flour a good candidate to provide healthier foods. Specifically, the presence of antioxidant compounds and the protein profile are expected to be related to reduced cardiovascular disease and hypoallergenic effects, respectively. In particular, einkorn was shown to express few T-cell stimulatory gluten peptides, with important implications for celiac disease [3]. In vitro digested einkorn breads evidenced their higher carotenoid level as compared to modern wheats and showed a greater anti-inflammatory effect than the control (wheat bread) in Caco-2 intestinal epithelial cells [4]. Given the crucial role of the gut microbiota in the metabolism of dietary compounds, including the bio-activation of plant polyphenols into health-promoting metabolites and the production of short-chain fatty acids (SCFAs, mainly acetate, propionate, and butyrate) from fiber fermentation, as major orchestrators of the host physiology [5].”

omissis….

“Specifically, for einkorn, one of the most representative ancient grains, in vitro results evidenced a good healthy potential because of its effects on blood concentrations of glucose and insulin with a view to using einkorn-based foods in metabolic diseases [7,8], but none has considered changes in the microbiota structure as well as in the intestinal repertoire of metabolites, potentially influencing multiple metabolic and immunological pathways that are relevant to host health. In an attempt to bridge this gap, here we explored the gut microbiota and metabolome of pigs fed with an einkorn versus wheat-based bread. “

omissis……

Conclusions. “In summary, through the pig model we demonstrated a beneficial impact of EB on several aspects of the host physiology, including insulin release, fecal consistency, and microbiota and metabolome profiles, both in feces and intestinal contents. According to our findings, the consumption of EB could reduce the AUC of the first insulin peak, thus prolonging the sense of satiety. Moreover, it could modulate the intestinal ecosystem, at both the compositional and metabolic scale, towards a configuration specifically enriched in health-promoting bacteria and showing distinct metabolic signatures potentially contributing to maintaining the host homeostasis. The use of the pig model allowed, unlike in clinical human trials, the sampling of the mucosa and the content of the small intestine, thus widening the knowledge on the complexity of the food-microbiota-host interaction along the gastrointestinal tracts. The observed positive effects could be driven by the synergistic interaction of many factors, including, inter alia, the fermentation process, the food matrix, and the flour components, which result in gut-mediated effects. The evaluation of the beneficial effects of a real food is far more complex than using purified compounds, as a direct cause-effect relationship can seldom be ascribed to a single component. It is indeed foods, and not the single components, which create the diet, and exploring their complexity can better reflect their overall role on health. Although further studies and clinical trials are needed, the results that are herein reported represent a first contribution to unravel the anti-inflammatory potential of einkorn-based foods.”

“In Vivo Effects of Einkorn Wheat (Triticum monococcum) Bread on the Intestinal Microbiota, Metabolome, and on the Glycemic and Insulinemic Response in the Pig Model”. Francesca Barone et al. Nutrients 2019, 11, 16; doi:10.3390/nu11010016

Note:
A – Pigs have significant anatomical and physiological similarities with humans, particularly with regard to the intestinal structure, with comparable transit time and analogous digestive and absorptive processes [9,10]. Furthermore, like humans, they are true omnivores, unlike other potential mammalian models, such as dogs, cats, ruminants, rabbits, and rodents, which have evolutionarily developed alternative digestive strategies. Finally, both pigs and humans are colon fermenters and have similar colonic microbiota composition. All of these features make the pig one of the most important models in the field of nutrition [11,12]. Through the pig model, in the present study we investigated the impact of a 30-day nutritional intervention with einkorn or wheat bread on the intestinal ecosystem, by means of next-generation sequencing of the 16S rRNA gene and metabolomics of fecal samples, as well as samples from ileal and colonic compartments. The effects of einkorn vs. wheat bread on animal physiology, blood parameters, postprandial glycemia, and insulin response were also evaluated.

B – The metabolome refers to the complete set of small-molecule chemicals found within a biological sample. The biological sample can be a cell, a cellular organelle, an organ, a tissue, a tissue extract, a biofluid or an entire organism. The small molecule chemicals found in a given metabolome may include both endogenous metabolites that are naturally produced by an organism (such as amino acids, organic acids, nucleic acids, fatty acids, amines, sugars, vitamins, co-factors, pigments, antibiotics, etc.) as well as exogenous chemicals (such as drugs, environmental contaminants, food additives, toxins and other xenobiotics) that are not naturally produced by an organism.
The metabolome refers to the complete set of small-molecule chemicals found within a biological sample. The biological sample can be a cell, a cellular organelle, an organ, a tissue, a tissue extract, a biofluid or an entire organism. The small molecule chemicals found in a given metabolome may include both endogenous metabolites that are naturally produced by an organism (such as amino acids, organic acids, nucleic acids, fatty acids, amines, sugars, vitamins, co-factors, pigments, antibiotics, etc.) as well as exogenous chemicals (such as drugs, environmental contaminants, food additives, toxins and other xenobiotics) that are not naturally produced by an organism.