Developmental Origins Of Health And Disease
The Developmental Origins of Health and Disease hypothesis posits that in utero or earlylife exposures influence ones susceptibility to chronic diseases later in life. Epidemiologic and animal models demonstrate the impact of the perinatal environment on programming longterm risk for chronic disease in offspring. Early studies associated low birthweight with increased cardiovascular disease mortality and hypertension in adulthood. This work, reported on a male UK cohort from almost 100 years ago, was the first to suggest that perinatal stress has both immediate implications for offspring and longterm impacts on adult health. Subsequent studies of the Dutch Hunger Winter and the Chinese Famine confirmed the association of gestational malnutrition with risk of chronic disease.
Mechanism Linking The Microbiota To Obesity
These shreds of evidence altogether have confirmed a statistical association between obesity and gut microbiota peculiar composition. A number of mechanisms has been proposed for gut microbiota causative action in obesity physiopathology. In fact, gut commensal bacteria interact with our metabolism at several points: it helps to convert ingested complex nutrients to SCFAs, transforms mucins and dietary fibers into simple sugars ready for absorption, stimulates intestinal epithelial proliferation, favors nutrients absorption and metabolism, it is the main actor in the shaping of gut crucial defense barrier constituted by systemic and mucosal immune system, and it activates bio-inactive compounds . Nevertheless, gut microbiota plays an important role in human adipose tissue formation and deposition. Indeed, our intestinal bacteria are able to maintain the human body energy balance mainly because of their ability to share otherwise indigestible components of mammalians diet .
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The Gut Microbiome’s Supersized Role In Shaping Molecules In Our Blood
- Institute for Systems Biology
- Scientists have shown which blood metabolites are associated with the gut microbiome, genetics, or the interplay between both. Their findings have promising implications for guiding targeted therapies designed to alter the composition of the blood metabolome to improve human health.
The nearly 200-year-old phrase “you are what you eat” has some new evidence. ISB researchers have found that the gut microbiome, including what we feed it, is largely responsible for the variation in circulating blood metabolites across people. This knowledge will help guide targeted interventions designed to alter the composition of the human blood metabolome.
“We know that person-to-person variation in the blood metabolome — the small molecules found in the bloodstream that can interact with all the systems of our body — can tell us a lot about health and disease status. Figuring out what governs this variation is a necessary step that gets us closer to precision approaches to healthcare,” said Dr. Sean Gibbons, an ISB faculty member and co-corresponding author of the paper.
Microbiome Changes Alter Th17 Cells
The reduction in filamentous bacteria, the researchers found, was critical to the animals health through its effect on Th17 immune cells. The drop in filamentous bacteria reduced the number of Th17 cells in the gut, and further experiments revealed that its the Th17 cells that are necessary to prevent metabolic disease, diabetes, and weight gain.
These immune cells produce molecules that slow down the absorption of bad lipids from the intestines and they decrease intestinal inflammation, Ivanov says. In other words, they keep the gut healthy and protect the body from absorbing pathogenic lipids.
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Fecal And Urine Sample Collection
Urine and fecal samples were collected after 26 months of dietary treatments. Animals were moved to metabolic cages with wire bottoms, and sample cups were checked every 15 min for feces. Fecal samples were immediately placed in sterile tubes under aseptic conditions and stored at 80 °C until further processing. As soon as adequate urine samples were available, they were collected, and stored at 80 °C until analysis.
Oral Administration Of D3 Counteracts Obesity
Increasing electric charge and hydrophobicity can improve the membrane permeability of peptides. Therefore, to enhance hydrophobicity, four peptides named D14 were modified from one of the fragments of HD5 degraded by proteases in human duodenal fluid, HD5, the first nine amino acids at the N-terminus of defensin HD5. All these peptides have a positive charge, among which D3 shows the strongest potential to penetrate cell membranes . We then evaluated the cytotoxicity of D14 in mammalian cells. D13 showed a slight inhibition of cell activity at a very high concentration , indicating their low cytotoxicity . Additionally, D14 was assayed for potential toxic effects on mouse red blood cells in vitro. As shown in , the haemolytic rate of D14 at 28µM was 1.06%3.61%, respectively, indicating their low haemolytic effect. Therefore, the safe concentration range of these small peptides was set to 027µM.
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Reduced Activity Of Fasting
Fasting-induced adipose factor is a circulating lipoprotein lipase inhibitor produced by the intestine, liver and adipose tissue . Gut microbiota efficiently suppress Fiaf expression in the ileum, enhancing the activity of LPL and increasing cellular uptake of fatty acids and storage of triglycerides in adipocytes . LPL is the key enzyme that acts on the endothelial surface of extra-hepatic capillaries, releasing large amounts of fatty acids from lipoproteins for the uptake of tissues for production or storage of energy . Bäckhed et al., demonstrated that hepatic lipogenesis appears to be induced in conventionalised GF-mice . The importance of Fiaf in this regulatory pathway was clarified by comparing GF- Fiaf knockout rodents to their wild-type littermates. In the absence of Fiaf, rodents gained substantially more weight than their littermates due to enhanced LPL activity. It is therefore possible that a reduction in Fiaf activity was responsible for the increased adiposity in CONV-D mice .
Perinatal Environment And Progression To Fibrosis In Offspring Nafld
Although multiple mouse models clearly demonstrate worse disease progression with maternal obesogenic diet exposure, this phenotype may be nutrient specific. For example, maternal HF/HSexposed offspring fed a NASHinducing diet were protected from fibrosis despite higher levels of hepatic TGs. Confirming this finding in other models will be essential for comparing epigenetic changes and identifying specific alterations leading to disease progression versus protection. There is precedent for transmitting protection from fibrosis across generations. Inducing fibrosis in male rats led to suppression of fibrosis development in filial 1 and F2 offspring through epigenetic changes that increased PPAR, a potential protective factor.
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Fibers And Short Chain Fatty Acids
The most widely studied metabolites include the short-chain fatty acids acetate, butyrate and propionate, generated by gut microbiota which ferment indigestible dietary components such as complex carbohydrates . In that regard, high fiber intake was associated with a protection from several metabolic diseases such as T2D . Further, fiber intake promoted the expansion of SCFAs producing bacteria and improved glucose tolerance in people with T2D . Inulin supplementation increased insulin sensitivity in human subjects. Inulin propionate ester improved insulin sensitivity as well as reduced IL-8 , suggesting beneficial effects on inflammatory parameters. Furthermore, high fiber intake promoted gut barrier integrity in mice, which was associated with the SCFAs production .
Future Manipulation Of Microbiota
As the evolving exploration for causality between obesity and microbiota continues, attention has been diverted to the search for techniques in microbiota manipulation with the objective of restoring a balanced gut microbiota community. FMT techniques have been refined and involve the transfer of carefully screened faecal material containing microbiota from a healthy donor into an identified diseased patient with the intention of cure . Probiotics and prebiotics are also proposed methods to manipulate the gut microbiota population in order to improve metabolic conditions, however FMT is considered to have the potential for being more successful. FMT has the ability to transfer entire donor microbiota communities, including their metabolites, to the identified recipient, with the perceived enhanced capability to correct microbiota disruption over single microbial targets such as probiotic supplementation .
Two randomised studies investigated the effects of using lean allogenic FMT in subjects diagnosed with metabolic syndrome . Both studies failed to show any improvement in metabolic parameters or subject physiology. However, it was noted that recipients of the lean allogenic FMT mostly, but not all were found to have gut microbiota composition that shifted towards an appearance similar to the donors profile implying unsuccessful engraftment .
Table 2 Faecal Microbiota Transplantation usage in human studies of obesity/metabolic syndrome
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One Study Found That We May Be Able To Achieve Higher Gut Microbiota Diversity By Increasing Our Fibre Intake
Pedersen says the reasons some people have more gut bacteria diversity than others isnt yet understood, but scientists do know that having multiple antibiotic treatments can contribute to a major loss of bacteria that never fully recovers.
It isnt fully established whether diversity of bacteria is a cause or consequence of weight gain, however, there is evidence that the microbiome can influence metabolism.
One study found that we may be able to achieve higher gut microbiota diversity . When we consume fibre, our guts break it down into short chain fatty acids, including butyrate, an anti-inflammatory linked to leanness and lower inflammatory diseases, explains Ana Valdes, author of the study and associate professor at the University of Nottingham.
If people with type 2 diabetes go on a high-fibre diet, you can reduce their diabetes status and increase butyrate production, she says.
People who have more diverse microbiomes and eat more fibre have less insulinogenic diets , and probably have higher energy expenditure.
Recent research suggests eating more fibre might help you achieve higher gut mircrobe diversity
We need to test this properly, but gut bacteria could convert the fibre into substances that modulate insulin sensitivity and energy metabolism.
When researchers looked at heritable gut microbes, Christensenellaceae came top of the list, found in gut microbiomes around the world and showing up from a very early age, including in the guts of babies.
Short Chain Fatty Acid Interaction With End
The SCFAs produced by the gut microbiota are absorbed into the bloodstream and reach distant tissues such as the liver, adipose tissue, and kidneys after their uptake by G protein-coupled receptors , including GPR41, GPR43, GPR109A, and Olf78. SCFAs differentially activate GPRs propionate activates GPR41 and GPR43, acetate activates GPR43, and butyrate activates GPR41 . Through the activation of GPR41 and 43 within adipocytes, epithelial and mononuclear cells, SCFAs initiate adipogenesis, suppress the synthesis of cholesterol and fatty acids in the liver, and regulate obesity in mice . In addition, GPR-41 activation improves blood pressure regulation, whereas GPR-43 activation enhances cell immune responses .
SCFA receptors and their relationship with different types of SCFAs.
GPR-109A may have an additional role in limiting inflammation . Animal and human studies have demonstrated an association between GPR109A expression and colon cancer, suggesting it may be a tumor suppressor . GPR109A activated by SCFAs also inhibits NF-kB activation and pancreatic beta cells inflammation in mice .
Unlike the other receptors, the Olfr-78 receptor does not respond to butyrate but is more sensitive to propionate and acetate . In addition to its role in olfaction and hormone regulation, Olfr-78 acts as a hypoxia sensor and plays a role in renin secretion and blood pressure regulation .
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Baseline Bmi And Weight Loss
In the present study, the researchers analyzed data from 105 individuals who had enrolled in a commercial behavioral wellness program.
The researchers collected information on the participants, including their weight and body mass index a value that a persons height and weight to estimate their body fat. They also looked at blood samples from both baseline and 612 months after the program began.
The researchers also collected dietary information and stool samples at the onset of the wellness program.
They used the blood samples to evaluate the levels of various metabolites and proteins and used the stool samples to determine gut microbiota composition and function.
The researchers also assessed differences in the function of the gut microbiota using metagenomic analysis. Instead of characterizing the genome of individual microorganism species, a metagenomic analysis involves identifying genes that are most abundant in the whole community of microorganisms that constitute the gut microbiota.
The identification of the most abundant genes can help predict the function of the entire gut microbiome.
Among the 105 participants, 48 individuals lost at least 1% of their weight per month, whereas the remaining 57 did not lose any weight.
The researchers identified the 15 individuals who lost the greatest amount of weight and the 10 people in the no-weight-loss group who showed the least significant change in their weight.
Oesophagus Stomach And Small Intestine
There are no data for permanent microbiota in the proximal part of the oesophagus. Studies have detected that in proximal oesophagus, the diversity of microbes is low. Studies for the distal part of the oesophagus say that there is reduced diversity and a dominant species of it is Streptococcus. Also, it is known that the reduced diversity of microbes in the oesophagus is good to sustain the wellbeing of the oesophagus . The low pH of stomach limits many types of microbes, which get there. Attendance or absence of Helicobacter pylori affects the composition of the stomach microbiota. When H. pylori are there, it is a dominant species. Otherwise, Streptococcus is dominant . H. pylori can be commensal or pathogen species of the stomach . Besides this, stomach microbiota consists of other species as Prevotella, Veillonella and Rothia.
It is very hard to derive data about the microbiota in the small intestine because of insufficiency of healthy volunteers. Based on some routine microbiological examinations and molecular studies, it is known that Streptococcus is a dominant species in duodenum and jejunum. Generally, it is accepted that the diversity and complexity of bacterial communities increases in proximal-distal direction .
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The Gut Microbiome Profile In Obesity: A Systematic Review
Olga CastanerHelmut Schröder
Gut microbiome has been identified in the past decade as an important factor involved in obesity, but the magnitude of its contribution to obesity and its related comorbidities is still uncertain. Among the vast quantity of factors attributed to obesity, environmental, dietary, lifestyle, genetic, and others, the microbiome has aroused curiosity, and the scientific community has published many original articles. Most of the studies related to microbiome and obesity have been reported based on the associations between microbiota and obesity, and the in-depth study of the mechanisms related has been studied mainly in rodents and exceptionally in humans. Due to the quantity and diverse information published, the need of reviews is mandatory to recapitulate the relevant achievements. In this systematic review, we provide an overview of the current evidence on the association between intestinal microbiota and obesity. Additionally, we analyze the effects of an extreme weight loss intervention such as bariatric surgery on gut microbiota. The review is divided into 2 sections: first, the association of obesity and related metabolic disorders with different gut microbiome profiles, including metagenomics studies, and second, changes on gut microbiome after an extreme weight loss intervention such as bariatric surgery.
2.1. Eligibility Criteria
3.1. Literature Search
Can We Prevent Obesity By Modulation Of The Gut Microbiota
Targeting microbiota may present new avenues for therapeutic interventions aimed at preventing or treating obesity and associated metabolic disorders. These strategies include dietary manipulation such as the use of prebiotics, probiotics or synbiotics, as well as transplantation of fecal microbial communities.
A prebiotic is a food ingredient that cannot be digested by the host and whose beneficial effects on the host result from the selective stimulation of growth and/or activity of the gut microbiota, particularly lactobacilli and bifidobacteria.24 Most of the attention in this area has been aimed at nondigestible oligosaccharides.25 Common prebiotics include inulin, other oligosaccharides, lactulose and resistant starch.24 In principle, all dietary fibers that are fermented are assumed to have prebiotic properties.24
In a double-blind, placebo-controlled, cross-over trial, consuming 30 grams isomalt per day for 4-weeks led to a 65% increase in the proportion of bifidobacteria and a 47% increase in total bifidobacteria cell counts compared to feeding sucrose.29 In another study in which 12 volunteers ingested 10 g inulin/day for 16 days in comparison to a control period without any supplement intake, Bifidobacterium adolescentis showed the strongest response, increasing from 0.89 to 3.9% of the total microbiota.30 Therefore, supplementing the diet with prebiotics can alter the gut microbial composition.
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