View clinical trials related to Gut Microbiota.
Filter by:Studies indicate that the intestinal microbiota could have an implication in Alzheimer's disease; recently, a positive relationship has been established between levels of bacterial lipopolysaccharide (LPS) and cerebral amyloidosis and a negative relationship between the production of the chain fatty acid cuts butyrate by the intestinal microbiota and cerebral amyloidosis. Currently there is no effective treatment for Alzheimer's, but studies indicate that a healthy diet such as the Mediterranean diet and physical exercise delay the symptoms of this disease. For all these reasons, it is postulated that introducing changes in the intestinal microbiota through diet may be a new treatment or serve as an adjuvant treatment for Alzheimer's disease.
Microbes and the human body maintain a complex relationship of interaction and influence. Different regions, altitudes, and dietary habits have different degrees of influence on the composition of children's intestinal flora. Therefore, the development and maturation process of children's intestinal flora in plateau areas was discovered, and its relationship with children's immunity, metabolism, and growth was understood. The mechanism of action of children's intestinal flora on immunity, growth and development was further analyzed by comparing it with people in low-altitude areas, to provide a scientific basis for improving children's health in plateau areas.
The Scottish Bowel Screening Programme is an enormous potential research resource; half a million people in Scotland do their bowel screening test each year. If we could obtain meaningful data on the gut microbiota in these individuals, many clinical questions could be answered using nested case-control studies relating gut microbiota profiles to cancer, obesity, cardiovascular and metabolic diseases and Alzheimer's disease. As individuals are screened from age 50 to 74 years, there would also be excellent opportunities for longer-term longitudinal studies. Since 2017, the bowel screening programme has used qFIT testing for faecal haemoglobin. Patients collect a tiny (2 miligram) sample of their faeces into 2 mililiter of buffer but only approximately 6 microliter is required for testing. The goal of this study is to investigate whether the large number of patients' samples available from the National Bowel Screening Programme could be used in future gut microbiome studies using the leftover faeces in buffer in the qFIT tests.
The role of intestinal microbiota is becoming ever more important in the context of obesity, type II diabetes (T2D), and infectious disorders as represented by the emerging discipline "therapeutic microbiology". The gut microbiota is strictly interconnected with obesity and T2D playing also an important role in immune system regulation. Obesity and diabetes can lead to chronic inflammation, which results in the secretion of pro-inflammatory cytokines like IL-6, IL-1, and TNF-alpha, causing immune system alteration which predisposes patients with obesity and T2D to chronic infections. Therefore, the principal aim of the study is to investigate changes in gut microbiota composition between patients with chronic infections or not, so as to attribute to specific phyla the formation of the infections in these patients.
It is observed that replacing meat with protein-rich plant-based food products are associated with lower mortality and obesity prevention. Sources of plant proteins typically undergo several processing and refinement procedures to improve the taste and digestibility of plant-based food products. These procedures alter the chemical composition, which can impact the nutritional quality of the processed food. It is not known what is the impact of processed products on human metabolism and intestinal microbiota. Therefore, the impact of a set of plant-based protein-rich food products with varying degree of processing on the composition and function of human gut microbiome and metabolism will be assessed in a clinical intervention
Undernutrition among women of reproductive age is more common in South Asia than in any other region. In South Asia, the prevalence of maternal undernutrition varies between 10 and 40%. There is a scarcity of data on the contribution of small intestinal (SI) microbiota to pathogenesis of Environmental Enteric Dysfunction (EED) of malnutrition, as it is difficult to obtain gut biopsy specimens from malnourished individuals, especially children. The Bangladesh Environmental Enteric Dysfunction (BEED) study, involving participants who live in an urban slum (Mirpur) in Dhaka, provided an opportunity to examine the role of the duodenal microbiota in the pathogenesis of EED in children and also performed esophagogastroduodenoscopy (EGD) on thirty-eight 18-45-year-old malnourished (BMI<18.5 kg/m2) women residing in the same resource-poor setting of Mirpur, Dhaka who failed to respond to a egg/milk/micronutrients-based nutritional intervention comparable to that given to children. In this intervention component, beginning at the end of the first trimester, low-BMI (<18.5 kg/m2) pregnant women (aged 18-30 years) will be randomly assigned to receive either the MDCF-2 or Ready-use-supplementary food (RUSF) for the duration of their pregnancy and during the first 3 postnatal months, in addition to standard antenatal care. A parallel cohort of age-matched normal-BMI pregnant women who will not receive any nutritional intervention will serve as a reference control group.
This research aims to elucidate an underlying mechanism of maternal obesity induced pregnancy and longterm health complications for mothers and their offspring.
Objective: To explore the predictive value of characteristic disorder of intestinal flora for clinical prognosis in patients with intracerebral hemorrhage. Secondary objectives: 1) To investigate the correlation of gut microbiota and its serological indicators with imaging features and clinical neurological deficits in ICH; 2) Dynamically observe the changes of human microbiome and its serological indicators after ICH, and explore the biomarkers based on human microbiome related to disease changes.
The objective of this study in healthy volunteers is to evaluate whether the composition of the gut microbiota and sleep quality influence the susceptibility to develop peripheral and central sensitization of pain pathways. In two different experimental sessions, the following factors will be tested: the influence of the composition of the gut microbiota on the susceptibility to develop peripheral sensitization of nociceptors, and the susceptibility to develop central sensitization of pain pathways. To assess susceptibility to peripheral sensitization, a solution of capsaicin (the active component of chili pepper) will be applied to the skin to induce neurogenic inflammation produced by the release of substances from nociceptors at the peripheral level. This neurogenic inflammation is characterized by a transient redness of the skin that will be measured with an infrared camera. To evaluate the susceptibility to sensitization at the central level, a high frequency electrical stimulation will be applied to the skin. This stimulation induces an increase in sensitivity to mechanical stimulation secondary to central sensitization. The intensity, extent and duration of this mechanical hyperalgesia will therefore be used as a measure of susceptibility to central sensitization. A stool sample and a blood sample will be taken. These samples will be used to characterize the composition of the intestinal microbiota, as well as the metabolites produced by this microbiota. These analyses will allow a comparison of the composition of the microbiota and the metabolites in subjects with a tendency to develop low vs. high sensitization at the peripheral and central levels. Similarly, sleep quality and average sleep duration will be assessed using questionnaires and a measurement of the participant's activity using a wrist movement sensitive bracelet. This information will be used to assess whether some of the interindividual variability in developing peripheral or central sensitization might be related to differences in sleep quality. Finally, systemic inflammation could be a factor modulated by sleep and gut microbiota, influencing pain perception and susceptibility to sensitization. For this reason, systemic pro- and anti-inflammatory cytokines will be measured in the blood sample.
Acute pancreatitis represents an acute inflammatory process of the pancreas, which undergoes local and systemic complications, associated with non-negligible morbidity and mortality, and significant economic and quality of life impact. Even after the recovery phase, the development and persistence of sequelae from the inflammatory/necrotic process, including exocrine and endocrine pancreatic insufficiencies, are frequent. Although well documented as consequence of other pancreatic conditions, exocrine pancreatic insufficiency (EPI) after acute pancreatitis is poorly studied and probably underdiagnosed. The prevalence, diagnosis, independent risk factors and therapeutic approaches for EPI after acute pancreatitis need further investigation. Recent evidence suggests the involvement of the pancreas-intestinal axis and immunological dysfunction in several pancreatic pathologies, although their role in the development of EPI after acute pancreatitis is still scarce. Pancreatic enzyme replacement therapy (PERT) is the only treatment currently available in EPI, but the timing for start and duration of this therapy in acute pancreatitis remain to be established. This study have the following objectives: to determine the prevalence, clinical, analytical and nutritional biomarkers and duration of EPI after acute pancreatitis, as well as changes in gut microbiota and immunologic response, and quality of life in EPI and response to PERT after acute pancreatitis; and to determine the prevalence and biomarkers associated with endocrine pancreatic insufficiency following acute pancreatitis and the presence of gut dysbiosis and immunologic changes in acute pancreatitis according to its severity.