Gut health for optimal metabolism -
Microbial gene richness might also have a role in the inflammatory status of the host, which is related to obesity. Individuals with obesity who have a high bacterial gene count were found to carry a higher proportion of species associated with an anti-inflammatory status for example, F.
prausnitzii and a lower proportion of species associated with a proinflammatory status for example, Bacteroides spp. Also, the bacterial gene count for genes associated with oxidative stress was higher in individuals with low bacterial gene count than in those with high bacterial gene count [ 51 ].
As carrying out a controlled dietary intervention study in humans is difficult, the complex interaction between diet, age, host environment, and host genetic background in the modulation of gut microbial ecosystems is not fully understood.
Nevertheless, a recent report suggests that alteration of the gut microbiota by behavioral changes, including new dietary habits [ 52 ] and use of antibiotics, could be the main driver of the obesity pandemic [ 53 , 54 ]. One of the hallmarks of obesity and obesity-related pathologies is the occurrence of chronic low-grade inflammation [ 22 ].
Lipopolysaccharides LPS , also called endotoxins, which are derived from the outer cell membrane of Gram-negative bacteria, have been thought to initiate the inflammation-related processes associated with the onset of obesity and insulin resistance Fig.
LPS contain lipid A in their structure and are able to cross the gastrointestinal mucosa via leaky intestinal tight junctions or by infiltrating chylomicrons, the lipoproteins responsible for the absorption of dietary triglycerides and cholesterol from the intestine to the plasma [ 23 , 55 , 56 ].
Once they reach the systemic circulation, LPS infiltrate tissues such as the liver or adipose tissues, triggering an innate immune response [ 23 ].
In particular, LPS bind the plasma LPS-binding protein LBP , which activates the receptor protein CD14 that is located in the plasma membrane of macrophages [ 56 ]. The complex thus generated binds Toll-like receptor 4 TLR4 at the surface of macrophages, which triggers transduction signals that activate the expression of genes encoding several inflammatory effectors, such as nuclear factor κB NF-κB and activator protein 1 AP-1 [ 56 , 57 ].
LPS also regulate the nucleotide oligomerization domain NOD -like receptors present in macrophages and dendritic cells, which cooperate with TLRs to induce NF-κβ. In addition, LPS participate in the recruitment of other effector molecules, such as nucleotide-binding domain leucine-rich repeat containing NLR protein, adaptor protein ASC, and caspase-1, which are components of the inflammasome, a multiprotein oligomer that activates the innate immune system [ 27 ].
Induction of inflammatory signals in proinflammatory macrophages and their connection with insulin pathways. a After translocation of gut bacteria to other tissues, the bacterial lipopolysaccharides LPS in the circulation and organs activate the transcription of cytokines via Toll-like receptor TLR 4.
Activated TLR4 mediates inflammatory signals involving myeloid differentiation primary response gene 88 MyD88 -dependent pathways. These pathways participate in the activation of transcription factors nuclear factor κB NF-κB and activator protein 1 AP-1 and cytokine production.
b Pattern-recognition receptors such as TLR4, TLR2, and TLR8 are activated by LPS, cytokines, or lipotoxicity. The intracellular nucleotide oligomerization domain NOD -like receptors also recognize LPS, which leads to induction of thioredoxin-interacting protein which is encoded by TXNIP and recruitment of other effector molecules such as those that are components of inflammasome pathways [ 28 ].
Inflammasomes are multiprotein complexes composed of three proteins: nucleotide-binding domain leucine-rich repeat containing NLR protein, adaptor protein ASC, and caspase Inflammasome activation contributes to the maturation of the cytokines interleukin IL -1β and IL Systemic LPS are found at low concentrations in healthy individuals but reach high concentrations in individuals with obesity, a condition called metabolic endotoxemia [ 23 ].
Several mechanisms linking obesity and metabolic endotoxemia have been proposed: during consumption of a high-fat diet, the gut microbiota is modified, which leads to increases in gut permeability and in the systemic levels of bacterial products such as LPS [ 23 ]. Additionally, excess fat intake triggers an increase in chylomicrons in the intestine during the postprandial period following a meal , which favors LPS infiltration into the circulation [ 58 ].
Impaired lipoprotein metabolism in patients with type 2 diabetes has also been found to reduce LPS catabolism and might increase endotoxemia-related inflammation [ 59 ]. The importance of metabolic endotoxemia in the physiopathology of insulin resistance and obesity has been further highlighted by Shi and colleagues [ 50 ], who showed that mice lacking TLR4 were protected against insulin resistance induced by a high-fat diet.
Results from another study revealed that LPS infusion into genetically identical male mice for 4 weeks induced a comparable weight gain to that observed in mice consuming a high-fat diet [ 23 ].
Circulating endotoxin levels were also associated with elevated TNF-α and IL-6 concentrations in adipocytes [ 62 ]. In addition, a high-fat or high-carbohydrate diet, but not a diet rich in fiber and fruit, activated systemic LPS secretion, as well as the expression of TLR4, NF-κB, and suppressor of cytokine SOC 3, which are factors also involved in pathways that regulate insulin secretion [ 62 ].
Together, these results show the important role LPS-mediated inflammatory pathways have in obesity and obesity-related pathologies. Other microbial-derived metabolites produced from aromatic amino acids tyrosine, tryptophan, and phenylalanine have been suggested to interact with host signaling pathways and thus affect host immunity.
Indole was identified as one of the major tryptophan-derived microbial metabolites [ 63 ], produced by the action of bacterial tryptophanase which is present in Bacteroides thetaiotaomicron , Proteus vulgaris , and Escherichia coli , among other species [ 64 ].
Upon absorption, indole can be sulfated in the liver, which results in the production of 3-indoxylsulfate, or can undergo further bacterial metabolism, leading to the production of a range of related compounds, including indolepyruvate, indolelactate, and indoleacetate [ 65 ].
These metabolites bind human pharmacological targets, which puts the impact of bacterial metabolism of tryptophan in human health and disease into a wider perspective.
In particular, 3-indoxylsulfate and indolepropionate have been thought to interact with inflammation-related processes in the human host [ 66 ]. Indolepropionate is a pregnane X receptor PXR agonist with a beneficial role in gut barrier function, which takes place either through up-regulation of the expression of junctional proteins or by downregulation of TNF-α production in enterocytes [ 66 ].
By improving intestinal barrier permeability, indolepropionate also indirectly limits the translocation of antigens and pathogens, and LPS infiltration, into the circulation and, therefore, might reduce metabolic endotoxemia and host inflammation [ 68 ].
Therefore, a healthy or dysbiotic gut microbiota affects the gut and metabolic health of the host through modulation of gut physiology and LPS infiltration, calorie intake, fat accumulation, and insulin action Fig.
Effects of a healthy gut microbiota and dysbiosis on the gut and metabolic health of the host. A healthy microbiota comprises a balanced representation of symbionts bacteria with health-promoting functions and pathobionts bacteria that potentially induce pathology.
Low bacterial gene counts have also been associated with altered gut microbial functions and dysbiosis and have been linked to increased fat accumulation, lipopolysaccharide-induced inflammation, insulin resistance, obesity, and the metabolic syndrome.
Individuals with these characteristics are more likely to develop metabolic diseases such as diabetes, cardiovascular diseases, and inflammatory bowel diseases. LBP LPS-binding protein, SCFA short-chain fatty acid. The study of the metabolic, signaling, and immune interactions between gut microbes and the host, and how these interactions modulate host brain, muscle, liver and gut functions, has raised the concept of therapeutic microbial manipulation to combat or prevent diseases [ 4 , 10 ].
In particular, the selection of specific gut bacterial strains and the enhancement of the gut microbial ecology represents a promising therapeutic approach to control energy intake and reduce the prevalence of obesity and the metabolic syndrome.
Fecal transplantation is an efficient way to reshape the gut microbial ecosystem after antibiotic treatment or to help fight intestinal infection with Clostridium difficile and can be used as therapy for inflammatory bowel diseases [ 69 , 70 ].
A study also showed that nine men with the metabolic syndrome who underwent fecal transplantation with stools from healthy lean individuals had lower fasting levels of triglycerides and developed greater hepatic and peripheral insulin sensitivity after transplantation than nine men who received a transplant of their own stool [ 71 ].
Therefore, fecal transplantation may be useful in the struggle against obesity, although the procedure is still at an experimental stage and the mechanisms involved require further understanding.
The use of probiotics and prebiotics to improve the interactions between gut microbes and host metabolism in obesity and other metabolic diseases has been extensively investigated [ 72 ]. Probiotics are live microorganisms that, when used as food supplements, beneficially affect the host by improving intestinal microbial balance and changing the composition of the colonic microbiota [ 73 ].
Specific bacterial species such as Bifidobacterium spp. have been shown to improve glucose homeostasis, reduce weight gain and fat mass, and restore glucose-mediated insulin secretion in mice fed a high-fat diet [ 73 ].
Prebiotics are composed of oligosaccharides or short-chain polysaccharides. They are found in common dietary products, such as vegetables and whole-grain cereals, and can be added in yoghurt.
The best-characterized prebiotics are fructosyl-oligosaccharides FOS , including inulin long-chain fructosyl-oligosaccharide , galactosyl-oligosaccharides GOS , and other oligosaccharides present in milk, which are transformed by the gut microbiota into SCFAs and simultaneously promote proliferation of selected commensal bacteria in the colon [ 74 — 77 ].
For example, inulin has been found to stimulate the growth of bifidobacteria and may reduce caloric intake and fat mass in animals H [ 75 ].
Prebiotic stimulation of the growth of bifidobacteria is correlated with increased glucose tolerance, improved glucose-induced insulin secretion, and normalization of inflammation in rodents [ 78 ]. GOS also modulate the uptake of monosaccharides from the gut by changing the activity of host monosaccharide transporters, which in turn results in activation of glycolytic pathways [ 76 ].
Consumption of prebiotics has also been associated with a reduction in hepatic, renal, and plasma lipid levels in rodents [ 74 , 75 ]. In particular, GOS supplementation in healthy mice decreased hepatic triglyceride levels by lowering the activity of lipogenic enzymes, fatty acid synthase, and microsomal triglyceride transfer proteins, which are involved in VLDL synthesis [ 75 , 79 ].
Therefore, ingestion of prebiotics might lower lipogenic activity and increase lipolytic activity. The effects of prebiotics and probiotics on anti-inflammatory pathways, weight gain, and glucose metabolism in rodents have been largely attributed to SCFA production [ 37 ].
SCFAs interact with GPCRs for example, GPR41 and GPR43 in the immune cells of the human colon and promote expression of specific chemokines in the colonic epithelium [ 80 , 81 ].
SCFAs repress NF-κB and affect the production of proinflammatory markers, such as IL-2 and IL, in leukocytes [ 82 ]. SCFAs enhance satiety by increasing the synthesis of PYY and proglucagon in epithelial cells and by inhibiting the expression of neuroendocrine factors such as leptin [ 83 ].
Other studies have indicated that the effects of prebiotics on intestinal health and inflammation are also mediated by the secretion of glucagon-like proteins GLP-1 and GLP-2 in enteroendocrine L cells [ 77 , 84 ]. These physiological changes were correlated with GLP-2 levels and disappeared when the mice were treated with a GLP-2 antagonist [ 68 ].
Another study also pointed out that a synbiotic treatment combining polydextrose and Bifidobacterium lactis B lowered the abundance of Porphyromonadaceae in mice fed a high-fat diet [ 85 ]. This dietary supplement is thought to inhibit T helper 17 T h 17 cell infiltration in the small intestine, preventing metabolic inflammation and the development of type 2 diabetes [ 85 ].
In humans, probiotic intervention studies have revealed a positive effect of these approaches on glucose metabolism [ 86 ]. For example, during a 6-week randomized placebo-controlled study of 60 overweight healthy Indian individuals, the VSL 3 probiotic mix decreased systemic glucose and insulin levels [ 87 ].
However, evidence of the anti-obesity effects of prebiotics remain to be demonstrated. Many human studies highlight moderate or no changes in weight loss after prebiotic interventions [ 88 ].
Randomized controlled studies have identified surrogate markers of prebiotic treatment such as plasma PYY, GLP-1, ghrelin to be negatively correlated with weight gain, inflammation, and impaired glucose metabolism, which support the mechanisms observed in rodents [ 89 , 90 ].
However, there is no evidence to suggest that prebiotic supplementation in infant formula improves growth or clinical outcomes or causes adverse effects in term infants.
Studies in children, adults, and the elderly vary in quality and outcomes. However, prebiotics have been shown to modulate the fecal microbiota and immune function in elderly individuals and to reduce the levels of markers of the metabolic syndrome in overweight adults [ 91 — 94 ].
The effect of prebiotics and probiotics in obesity and related pathologies in humans requires further exploration. In particular, carefully designed studies using appropriate doses of probiotics or prebiotics and controlled diets will be valuable to underpin the individual responses to different types of interventions and their dependence on genetic, environmental, and gut microbial factors.
The evidence for a strong contribution of the gut microbiota to the onset of obesity and metabolic diseases is growing. The use of germ-free rodent models has enabled us to establish the molecular basis of the interactions between gut microbes and the physiology of the host.
The modifications in the gut microbial ecology by dietary factors, antibiotics, probiotics, or prebiotics that were observed in rodents and humans have further highlighted the key modulatory roles of the gut microbiota and its contribution to host obesity and metabolic diseases.
In particular, some metabolic disorders of the host are thought to be associated with an inflammation-related composition of the gut microbiota. However, how external factors such as diet, stress, age, drug intake, and circadian cycles affect the gut microbial composition and the effectiveness of microbial functions in rodents and humans is still unclear.
In the future, it seems essential to promote top-down analytical approaches on an epidemiological scale, integrating data from dietary questionnaires, data about relevant environmental factors such as stress or factors that influence circadian rhythms and history of drug or antibiotic use to understand more deeply the functions of gut bacteria in the physiopathology of human obesity.
In combination with animal studies, these integrated epidemiological analyses will enable us to unravel the missing connections within the metabolic axis linking gut microbes and the host and to optimize therapeutic strategies to reshape the gut microbial ecology.
Using this knowledge, we also hope to improve the stratification of populations at risk of developing metabolic diseases and offer novel perspectives for personalized healthcare, within which clinicians might be able to tailor therapy on the basis of individual habits and predispositions.
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This story is from September 18, Those looking for tips to improve gut health and metabolism, this article is for you, as it highlights five foods that can enhance digestion and promote gut health. From Greek yoghurt's probiotics, ginger's anti-inflammatory properties, and fibre-rich foods, there are several such foods that can regulate bowel movements.
Also, if you want to improve metabolism, there are some simple tips that you can incorporate in your life. However, diets high in saturated fats and low in fiber could disrupt the microbiome and lead to weight gain and sluggish metabolism.
Moreover, an unhealthy gut can cause GI distress, bloating, and discomfort. Have you struggled to lose weight despite following a low-fat diet and exercising regularly?
A slow metabolism or imbalance in gut bacteria can also contribute to weight gain. The solution lies in understanding how your body absorbs nutrients and converts them into energy. Focusing on a balanced diet that includes healthy fats, protein, and complex carbohydrates can help optimize nutrient absorption and improve energy production.
In opposition, a fast metabolism is often viewed as the key to effective weight control. A faster metabolic rate can burn calories quicker, preventing weight gain and promoting weight loss. Consuming a well-balanced diet rich in proteins, whole grains, fruits, and vegetables is just as crucial for people with a fast metabolism.
Regular physical activity can also help in maintaining a fast metabolism. Additionally, taking care of your gut health by consuming probiotics and prebiotics can regulate your gastrointestinal tract GI and boost your metabolism. You can see real progress in your weight loss journey by addressing these underlying issues.
Maintaining a healthy lifestyle is crucial for maintaining metabolic health and preventing weight gain. Many of us struggle with losing weight despite following a low-fat diet and exercising regularly and often blame our slow metabolism.
Jump to: What is the microbiome? Ophimal areas of research. Picture a Body shape confidence city on a weekday morning, the sidewalks flooded with people rushing hfalth get metaboliem work or Blood circulation supplements appointments. Ehalth imagine this at optmial microscopic level and Metabolidm have an idea of what the microbiome looks like inside our bodies, consisting of trillions of microorganisms also called microbiota or microbes of thousands of different species. The microbiome is even labeled a supporting organ because it plays so many key roles in promoting the smooth daily operations of the human body. The microbiome consists of microbes that are both helpful and potentially harmful. Most are symbiotic where both the human body and microbiota benefit and some, in smaller numbers, are pathogenic promoting disease. Poor Body shape confidence health may manifest fir fatigue, upset stomach, skin optijal, and emtabolism challenges. Mmetabolism, fermented foods, hydration, and Astaxanthin and liver health management can help. Each person has about different species of bacteria, viruses, and fungi in their digestive tract. Some microorganisms are harmful to our health, but many are incredibly beneficial and even necessary for a healthy body. Research indicates that having a large variety of bacteria in the gut may help reduce the risk of conditions like:.
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