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Perna canaliculus (Green-Lippped Mussel) is found only in New Zealand waters and is cultivated and manufactured for both the food and nutraceutical industry world-wide. P. canaliculus has traditionally been used as a therapeutic to treat various arthralgias in both humans and animals; however, clinical research reports provide conflicting results. Numerous in vitro studies have reported anti-inflammatory activity of the mussel under various conditions and also demonstrated a synergistic effect with pharmaceutical medications such as non-steroidal anti-inflammatory drugs (NSAIDs) with P. canaliculus protecting the gastrointestinal mucosal lining against such medications. It is proposed that the anti-inflammatory activity demonstrated by P. canaliculus is predominantly due to the lipid fraction, however, among the major classes of compounds found in mussel meat, proteins and peptides are the largest with isolates demonstrating various anti-microbial, anti-inflammatory, anti-oxidant, bioadhesive and anti-hypertensive activities. A review of the bioactive components, their function and therapeutic application is outlined in this chapter. Furthermore, we hypothesise and provide supportive evidence that the gastrointestinal microbiota play an important role in disease processes such as Rheumatoid arthritis and Osteoarthritis and also in the efficacy of P. canaliculus in chronic inflammatory conditions. The metabolic capacity of intestinal microbiota can modify bioactive food components altering the hosts' exposure to these components, potentially enhancing or diminishing their health effects. Understanding the interaction of the bioactive compounds in P. canaliculus with commensal and pathogenic bacteria may facilitate the development of novel interventions to control intestinal and extraintestinal inflammation.
Assuntos
Artrite/tratamento farmacológico , Inflamação/tratamento farmacológico , Perna (Organismo) , Animais , Antiasmáticos/farmacologia , Anti-Inflamatórios/farmacologia , Doença Crônica , Humanos , Intestinos/microbiologia , Microbiota , Perna (Organismo)/químicaRESUMO
Bacteria represent the earliest form of independent life on this planet. Bacterial development has included cooperative symbiosis with plants (e.g., Leguminosae family and nitrogen fixing bacteria in soil) and animals (e.g., the gut microbiome). It is generally agreed upon that the fusion of two prokaryotes evolutionarily gave rise to the eukaryotic cell in which mitochondria may be envisaged as a genetically functional mosaic, a relic from one of the prokaryotes. This is expressed by the appearance of mitochondria in eukaryotic cells (an alpha-proteobacteria input), a significant endosymbiotic evolutionary event. As such, the evolution of human life has been complexly connected to bacterial activities. Hence, microbial colonization of mammals has been a progressively driven process. The interactions between the human host and the microbiome inhabiting the gastrointestinal tract (GIT) for example, afford the human host the necessary cues for the development of regulated signals that in part are induced by reactive oxygen species (ROS). This regulated activity then promotes immunological tolerance and metabolic regulation and stability, which then helps establish control of local and extraintestinal end-organ (e.g., kidneys) physiology. Pharmacobiotics, the targeted administration of live probiotic cultures, is an advancing area of potential therapeutics, either directly or as adjuvants. Hence the continued scientific understanding of the human microbiome in health and disease may further lead to fine tuning the targeted delivery of probiotics for a therapeutic gain.
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Bactérias/isolamento & purificação , Trato Gastrointestinal/microbiologia , Probióticos/uso terapêutico , Animais , Humanos , Higiene , Tolerância Imunológica , MicrobiotaRESUMO
Individual participant data meta-analyses enable detailed checking of data quality and more complex analyses than standard study-level synthesis of summary data based on publications. However, there is limited existing guidance on the specific systematic checks that should be undertaken to confirm and enhance data quality for individual participant data meta-analyses and how to conduct these checks. We aim to address this gap by developing a checklist of items for data quality checking and cleaning to be applied to individual participant data meta-analyses of randomised trials. This study will comprise three phases: 1) a scoping review to identify potential checklist items; 2) two e-Delphi survey rounds among an invited panel of experts followed by a consensus meeting; and 3) pilot testing and refinement of the checklist, including development of an accompanying R-markdown program to facilitate its uptake.
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Lista de Checagem , Confiabilidade dos Dados , Consenso , Técnica Delphi , Humanos , Metanálise como Assunto , Ensaios Clínicos Controlados Aleatórios como AssuntoRESUMO
Early treatment may prevent or delay the onset of type 2 diabetes mellitus (T2DM) in individuals who are at high risk. Lifestyle interventions and the hypoglycemic drug metformin have been shown to reduce T2DM incidence. The effectiveness of such interventions may be enhanced by targeting environmental factors such as the intestinal microbiota, which has been proven to predict the response to lifestyle interventions and play a part in mediating the glucose-lowering effects of metformin. Shifts in the intestinal microbiota "towards a more balanced state" may promote glucose homeostasis by regulating short-chain fatty acids' production. This study aimed to investigate the safety and effect of a multi-strain probiotic on glycemic, inflammatory, and permeability markers in adults with prediabetes and early T2DM and to assess whether the probiotic can enhance metformin's effect on glycaemia. A randomised controlled pilot study was conducted in 60 adults with a BMI ≥ 25 kg/m2 and with prediabetes or T2DM (within the previous 12 months). The participants were randomised to a multi-strain probiotic (L. plantarum, L. bulgaricus, L. gasseri, B. breve, B. animalis sbsp. lactis, B. bifidum, S. thermophilus, and S. boulardii) or placebo for 12 weeks. Analyses of the primary outcome (fasting plasma glucose) and secondary outcomes, including, but not limited to, circulating lipopolysaccharide, zonulin, and short chain fatty acids and a metagenomic analysis of the fecal microbiome were performed at baseline and 12 weeks post-intervention. The results showed no significant differences in the primary and secondary outcome measures between the probiotic and placebo group. An analysis of a subgroup of participants taking metformin showed a decrease in fasting plasma glucose, HbA1c, insulin resistance, and zonulin; an increase in plasma butyrate concentrations; and an enrichment of microbial butyrate-producing pathways in the probiotic group but not in the placebo group. Probiotics may act as an adjunctive to metformin by increasing the production of butyrate, which may consequently enhance glucose management.
Assuntos
Glicemia/análise , Diabetes Mellitus Tipo 2/sangue , Microbioma Gastrointestinal , Hipoglicemiantes/administração & dosagem , Metformina/administração & dosagem , Probióticos/administração & dosagem , Idoso , Bacteroidetes/fisiologia , Butiratos/sangue , Ácidos Graxos Voláteis/sangue , Feminino , Firmicutes/fisiologia , Microbioma Gastrointestinal/efeitos dos fármacos , Haptoglobinas , Humanos , Resistência à Insulina , Masculino , Redes e Vias Metabólicas/efeitos dos fármacos , Pessoa de Meia-Idade , Projetos Piloto , Estado Pré-Diabético/sangue , Probióticos/efeitos adversos , Probióticos/farmacologia , Precursores de Proteínas/sangue , Proteobactérias/fisiologiaRESUMO
Adverse fluctuations in the distribution of the intestinal microbiome cohort has been associated with the onset of intra- and extra-intestinal inflammatory conditions, like the metabolic syndrome (MetS) and it's hepatic manifestation, non-alcoholic fatty liver disease (NAFLD). The intestinal microbial community of obese compared to lean subjects has been shown to undergo configurational shifts in various genera, including but not limited to increased abundances of Prevotella, Escherichia, Peptoniphilus, and Parabacteroides and decreased levels of Bifidobacteria, Roseburia, and Eubacteria genera. At the phylum level, decreased Bacteroidetes and increased Firmicutes have been reported. The intestinal microbiota therefore presents an important target for designing novel therapeutic modalities that target extra-intestinal inflammatory disorders, such as NAFLD. This review hypothesizes that disruption of the intestinal-mucosal macrophage interface is a key factor in intestinal-liver axis disturbances. Intestinal immune responses implicated in the manifestation, maintenance and progression of NAFLD provide insights into the dialogue between the intestinal microbiome, the epithelia and mucosal immunity. The pro-inflammatory activity and immune imbalances implicated in NAFLD pathophysiology are reported to stem from dysbiosis of the intestinal epithelia which can serve as a source of hepatoxic effects. We posit that the hepatotoxic consequences of intestinal dysbiosis are compounded through intestinal microbiota-mediated inflammation of the local mucosa that encourages mucosal immune dysfunction, thus contributing important plausible insight in NAFLD pathogenesis. The administration of probiotics and prebiotics as a cure-all remedy for all chronic diseases is not advocated, instead, the incorporation of evidence based probiotic/prebiotic formulations as adjunctive modalities may enhance lifestyle modification management strategies for the amelioration of NAFLD.
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Traditionally recognized as mental illnesses, eating disorders are increasingly appreciated to be biologically-driven. There is a growing body of literature that implicates a role of the gut microbiota in the etiology and progression of these conditions. Gut bacteria may act on the gut-brain axis to alter appetite control and brain function as part of the genesis of eating disorders. As the illnesses progress, extreme feeding patterns and psychological stress potentially feed back to the gut ecosystem that can further compromise physiological, cognitive, and social functioning. Given the established causality between dysbiosis and metabolic diseases, an altered gut microbial profile is likely to play a role in the co-morbidities of eating disorders with altered immune function, short-chain fatty acid production, and the gut barrier being the key mechanistic links. Understanding the role of the gut ecosystem in the pathophysiology of eating disorders will provide critical insights into improving current treatments and developing novel microbiome-based interventions that will benefit patients with eating disorders.
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Ingestão de Alimentos/fisiologia , Transtornos da Alimentação e da Ingestão de Alimentos/microbiologia , Microbioma Gastrointestinal/fisiologia , Disbiose , Transtornos da Alimentação e da Ingestão de Alimentos/patologia , HumanosRESUMO
BACKGROUND: Shifts in the gastrointestinal microbiome have been shown to contribute to the progression of metabolic diseases including prediabetes and type 2 diabetes mellitus. Research suggests that in-vivo modulation of the gut microbiome by specific probiotic microorganisms may improve insulin sensitivity and blood sugar management, preventing or delaying the development of type 2 diabetes mellitus. However, further research is needed to understand the effect of probiotics as a therapy for the treatment of metabolic diseases. An evidence-based multi-species probiotic was developed to encourage a shift in the gastrointestinal bacterial cohort from a disease-prone to a balanced state with the aim of improving metabolic markers associated with type 2 diabetes mellitus. METHODS: Sixty adults with a body mass index ≥25 kg/m2 with prediabetes or type 2 diabetes mellitus (diagnosed within the previous 12 months) will be enrolled in a double-blind, placebo-controlled pilot study. Participants will be randomized to a multi-species probiotic or placebo for 12 weeks. Both groups will receive lifestyle and nutritional advice. The primary outcome measure is the change between groups in fasting plasma glucose levels from baseline to 12 weeks. Secondary outcome measures include, but are not limited to, the change in lipid profile, systemic inflammation, gut permeability, and faecal microbial and metabolomic profiles. Blood and stool samples are collected at baseline and 12 weeks after treatment. DISCUSSION: Intentional manipulation of gastrointestinal microbial profiles may be useful for preventing and controlling type 2 diabetes mellitus and its associated metabolic complications. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry, ACTRN12613001378718 . Registered on 16 December 2013.