Diet- microbiota interactions as moderators of human metabolism : Nature : Nature Research. Extensive research on the gut microbiota has shown that diet modulates the composition and function of this community of microbes in humans and other mammals. Human intervention studies from the past decade have revealed the extent to which different aspects of the microbiota can be influenced through dietary change; this can be summarized by three main themes. The first theme is that the microbiota of the human gut responds rapidly to large changes in diet. The existence of these fast, diet- induced dynamics is supported by evidence from people who switch between plant- and meat- based diets, who add more than 3. Such marked shifts in response to nutrient availability are perhaps unsurprising given that populations of microbes can double within an hour and the gut extensively purges the community every 2. This responsiveness might represent an advantageous feature of enlisting microbes as part of the digestive structure — especially when considering the possible day- to- day variation in food that is available to foragers. It might also be an inescapable consequence of dealing with a complex and competitive microbial community that undergoes rapid turnover. The second theme is that, despite these rapid dynamics, long- term dietary habits are a dominant force in determining the composition of an individual's gut microbiota. Despite detectable responses of the microbiota within 2. Some, but not all, cross- sectional studies reported that long- term dietary trends are linked to features of microbiota composition. The third theme is that a particular change in diet can have a highly variable effect on different people owing to the individualized nature of their gut microbiota. For example, Ruminococcus bromii- related taxa bloomed in response to resistant- starch intervention in most of the 1. A dietary intervention that includes a boosted intake of fibre and a decreased intake of energy can increase microbiota diversity — as defined by the gene content of the faecal metagenome — for individuals who start with a low microbiota gene content, but not those who start with a high gene content. These individualized responses might fit into categories that enable a precision rather than a personalized approach to understanding responsiveness to diet. The influence of diet on aspects of microbiota function might also help to explain how a specific metabolic input can alter microbiota composition over time. In a study that focused on the enzymatic activity of trimethylamine lyase, mice that harbour microbiotas with low production of trimethylamine (TMA) could be converted into high producers when their diet was supplemented with the TMA- containing compound L- carnitine for 1. Similarly, a microbiota- encoded degradation system for porphyran, a polysaccharide that is found in certain species of edible seaweed, is rare in the microbiotas of Western people but prominent in those of populations that regularly consume seaweed. This suggests that certain metabolic inputs can select for pathways as well as the organisms that harbour those pathways. One corollary of this interpretation is that there must be a reservoir of selectable functions — either present at low levels within the gut microbial community or able to invade from an environmental source. It is important to note that numerous other non- dietary mechanisms, such as interstrain killing that is mediated by the type VI secretion system, infection with bacteriophages and priority effects of colonization through which strains are able to exclude one another on the basis of relatedness of particular genetic loci, can underlie microbial community dynamics and might interact with or operate in parallel to dietary- mediated effects. Several issues can complicate the unravelling of mechanisms and the interpretion of data in dietary intervention studies in humans. People are notoriously poor at adhering to dietary regimes, and it is difficult to accurately measure the extent of their adherence because the self- assessment of food intake can be clouded by numerous factors. Budget limitations often mean that researchers must choose either tightly controlled studies of small cohorts, for example, in which food is provided, or larger cohort studies that could be confounded by the free will of the participants and by their self- assessment. Metabolism involves a vast array of chemical reactions, but most fall under a few basic types of reactions that involve the transfer of functional groups of atoms and. The pathway of glycolysis as it is known today took almost 100 years to fully discover. The combined results of many smaller experiments were required in. The metabolism of people with diabetes differs to the metabolism of people without it. In type 2 diabetes, the effectiveness of insulin is reduced and in type 1. Because dietary change often involves both the elimination and addition (that is, the substitution) of dietary components, even the most successful intervention studies can raise questions about which diet modification was responsible for the change in the microbiota. A further complication is that many of the dietary changes in such studies also have the potential to directly influence host metabolism in a microbiota- independent way. As an alternative, animal models enable researchers to tightly control the diet of subjects and to have multiple biological replicates that represent the response of a single microbiota. Experimental models that lack a gut microbiota offer further power for determining whether the effects of diet in the host depend on the microbiota. For example, germ- free rats harvest less energy from a polysaccharide- rich diet. These results are consistent with the fact that the fermentation of dietary fibre represents one of the dominant microbial metabolic activities in the colon, the region of the gut in which the microbiota is most dense. The short- chain fatty acid end- products of fermentation in the gut can be absorbed into the circulation to serve as both microbiota- generated calories and important regulatory molecules, and it has been estimated that people who consumed a typical British diet in the 1. By contrast, people who eat large quantities of plants, the main source of dietary fibre. African communities that consume up to sevenfold more fibre than people the industrialized world. This is in agreement with the increased abundance of taxa that ferment polysaccharides in the gut microbiota of African populations. Certain recurrent physiological states in mammals, such as the non- hibernating period in bears. It should also be noted that the effects observed in animal models extend beyond a simple improvement in calorie harvest. The microbiota of mice suppress the expression of intestinal angiopoietin- like protein 4, an inhibitor of the enzyme lipoprotein lipase, which increases lipoprotein- lipase activity in adipose tissue and promotes the storage of fat. Accordingly, mice that are deficient in Angptl. Experiments that use a Western- style diet, which is devoid of fibres and rich in calories from saturated fat and sucrose, demonstrate that the gut microbiota regulates obesity through additional pathways. For example, germ- free mice are protected from diet- induced obesity when fed high levels of sucrose and lard. The presence of the microbiota is both necessary and sufficient for obesity: the transfer of microbiota from mice fed a Western diet to germ- free mice transfers the obese phenotype. By contrast, germ- free mice that are fed a high- fat diet with less sucrose are only partly protected against obesity. The molecular mechanisms that underpin this finding are unknown. The source of dietary fat also seems to be important. Saturated and unsaturated fats have profoundly different effects on the gut microbiota, and the altered microbiota that results from feeding unsaturated fats can offer protection from lard- induced weight gain. These findings suggest that simple carbohydrates and fats could exert unexpected effects on the host metabolism through the microbiota. Further research is required to clarify how microbial taxa and ecosystems interact with specific macronutrients. Emerging evidence suggests that the deleterious metabolic effects of processed foods might involve more than just macronutrients. Cell Metabolism will be holding editorial office hours on April 27, where the editors will be available from 10 to 11 a.m. EST and from 2 to 3 p.m. Introduction Sleep loss can occur as a result of habitual behavior or due to the presence of a pathological condition that is associated with reduced total sleep. Research on major depression has confirmed that it is caused by an array of biopsychosocial and lifestyle factors. Diet, exercise and sleep are three such. Emulsifiers and artificial sweeteners have been shown to be involved in the development of metabolic syndrome features through their modulation of the microbiota in mice. In a study in seven people, artificial sweeteners given at high doses resulted in insulin resistance after only 7 days. These data provide evidence that artificial food additives might contribute to metabolic disease through disruption of the microbiota. Notably, an important and unwavering commonality of Western dietary trends is the paucity of plant- based dietary fibre. The absence of dietary fibre together with an abundance of nutrients that negatively affect the microbiota could be of considerable importance for understanding metabolic diseases. The Ketogenic Diet's Effect on Cortisol Metabolism. Glycogen is a polymer of glucose residues linked mainly by a(1®4) glycosidic linkages. There are a(1®6) linkages at branch points. The chains and branches are. Metabolism Volume 71, In Progress Volume / Issue In ProgressA Volume/Issue that is "In Progress" contains final, fully citable articles that are published online, but. The ethanol metabolism page describes the mechanisms and regulation of this process as well as the consequences of acute and chronic alcohol consumption.
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