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1.
  • Bäckhed, Fredrik, 1973 (creator_code:aut_t)
  • 99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: the normal gut microbiota in health and disease.
  • 2010
  • record:In_t: Clinical and experimental immunology. - : Oxford University Press (OUP). - 1365-2249 .- 0009-9104. ; 160:1, s. 80-4
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • Mammals are metagenomic, in that they are composed not only of their own genome but also those of all of their associated microbes (microbiome). Individual variations in the microbiome influence host health and may be implicated in disease aetiology. Therefore, it is not surprising that decreased microbial diversity is associated with both obesity and inflammatory bowel disease. Studies in germ-free mice have demonstrated that the gut microbiota is required for development of diet-induced obesity as well as inflammatory diseases. However, the underlying molecular mechanism(s) for how the gut microbiota causes metabolic diseases is only beginning to be clarified. Furthermore, emerging data suggest that the gut microbiota may predispose or protect against other important diseases such as cardiovascular disease and diabetes.
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3.
  • Bäckhed, Fredrik, 1973, et al. (creator_code:aut_t)
  • Coordinated regulation of the metabolome and lipidome at the host-microbial interface
  • 2010
  • record:In_t: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1801:3
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • The creative use of gnotobiotic animals, coupled with the development of modern metagenomic sequencing platforms and metabolomic profiling of biospecimens, has bestowed new insight into the remarkably intricate interface between the host mammal and its resident microbiota. As mutual benefactors, each partner exhibits evidence of adaptation: the host provides a hospitable habitat, giving consideration to its own species of origin, diet, genotype, geographical location, presence or absence of disease, and use of medications; the microbiota, in turn, configures its constituency, collective genome (microbiome), transcriptome, and metabolome to optimally suit its ecological niche. In this review, we discuss the mechanisms through which the gut microbiota and its host collaborate to regulate lipid metabolism, thereby influencing the metabolic response to nutrient intake and ultimately, the development of obesity and associated diseases such as lipotoxicity. These studies therefore demonstrate that the gut microbiota is an 'environmental' influence whose synergistic interdependence with its host strongly suggests that we are in fact 'supraorganisms'.
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4.
  • Bäckhed, Fredrik, 1973, et al. (creator_code:aut_t)
  • Host-bacterial mutualism in the human intestine
  • 2005
  • record:In_t: Science. ; 307:5717, s. 1915-20
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • The distal human intestine represents an anaerobic bioreactor programmed with an enormous population of bacteria, dominated by relatively few divisions that are highly diverse at the strain/subspecies level. This microbiota and its collective genomes (microbiome) provide us with genetic and metabolic attributes we have not been required to evolve on our own, including the ability to harvest otherwise inaccessible nutrients. New studies are revealing how the gut microbiota has coevolved with us and how it manipulates and complements our biology in ways that are mutually beneficial. We are also starting to understand how certain keystone members of the microbiota operate to maintain the stability and functional adaptability of this microbial organ.
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5.
  • Bäckhed, Fredrik, 1973, et al. (creator_code:aut_t)
  • Toll-like receptor 4-mediated signaling by epithelial surfaces: necessity or threat?
  • 2003
  • record:In_t: Microbes Infect. ; 5:11, s. 951-9
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • Recent data suggest that the lipopolysaccharide receptor Toll-like receptor (TLR) 4 is expressed by epithelial cells and might play a role in the mucosal host defense against Gram-negative bacteria. However, since many body surfaces are colonized by the physiological microflora, activation of epithelial TLRs must be tightly controlled to avoid unintended stimulation and mucosal inflammation. The present review summarizes the current understanding of TLR4-mediated recognition and addresses specific questions on microbial recognition on mucosal surfaces, with particular emphasis on the gastrointestinal and urinary tract.
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6.
  • Delzenne, Nathalie, et al. (creator_code:aut_t)
  • Targeting gut microbiota in obesity: effects of prebiotics and probiotics
  • 2011
  • record:In_t: Nature reviews. Endocrinology. - : Springer Science and Business Media LLC. - 1759-5029 .- 1759-5037. ; 7:11, s. 639-646
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • At birth, the human colon is rapidly colonized by gut microbes. Owing to their vast number and their capacity to ferment nutrients and secrete bioactive compounds, these gastrointestinal microbes act as an environmental factor that affects the host's physiology and metabolism, particularly in the context of obesity and its related metabolic disorders. Experiments that compared germ-free and colonized mice or analyzed the influence of nutrients that qualitatively change the composition of the gut microbiota (namely prebiotics) showed that gut microbes induce a wide variety of host responses within the intestinal mucosa and thereby control the gut's barrier and endocrine functions. Gut microbes also influence the metabolism of cells in tissues outside of the intestines (in the liver and adipose tissue) and thereby modulate lipid and glucose homeostasis, as well as systemic inflammation, in the host. A number of studies describe characteristic differences between the composition and/or activity of the gut microbiota of lean individuals and those with obesity. Although these data are controversial, they suggest that specific phyla, classes or species of bacteria, or bacterial metabolic activities could be beneficial or detrimental to patients with obesity. The gut microbiota is, therefore, a potential nutritional and pharmacological target in the management of obesity and obesity-related disorders.
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7.
  • Enav, H., et al. (creator_code:aut_t)
  • The developing infant gut microbiome: A strain-level view
  • 2022
  • record:In_t: Cell Host and Microbe. - : Elsevier BV. - 1931-3128. ; 30:5, s. 627-638
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • At birth, neonates provide a vast habitat awaiting microbial colonization. Microbiome assembly is a complex process involving microbial seeding and succession driven by ecological forces and subject to environmental conditions. These successional events not only significantly affect the ecology and function of the microbiome, but also impact host health. While the establishment of the infant microbiome has been a point of interest for decades, an integrated view focusing on strain level colonization has been lacking until recently. Technological and computational advancements enabling strain-level analyses of the infant microbiome have demonstrated the immense complexity of this system and allowed for an improved understanding of how strains of the same species spread, colonize, evolve, and affect the host. Here, we review the current knowledge of the establishment and maturation of the infant gut microbiome with particular emphasis on newer discoveries achieved through strain-centric analyses.
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8.
  • Greiner, Thomas U., 1977, et al. (creator_code:aut_t)
  • Effects of the gut microbiota on obesity and glucose homeostasis.
  • 2011
  • record:In_t: Trends in endocrinology and metabolism: TEM. - : Elsevier BV. - 1879-3061 .- 1043-2760. ; 22:4, s. 117-23
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • The human gut is home to a vast number of bacteria, the microbiota, whose genomes complement our own set of genes. The gut microbiota functions at the intersection between host genotype and diet to modulate host physiology and metabolism, and recent data have revealed that the gut microbiota can affect obesity. The gut microbiota contributes to host metabolism by several mechanisms including increased energy harvest from the diet, modulation of lipid metabolism, altered endocrine function, and increased inflammatory tone. The gut microbiota could thus be considered to be an environmental factor that modulates obesity and other metabolic diseases.
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9.
  • Reinhardt, Christopher, et al. (creator_code:aut_t)
  • Intestinal microbiota during infancy and its implications for obesity
  • 2009
  • record:In_t: Journal of Pediatric Gastroenterology and Nutrition. - 1536-4801. ; 48:3, s. 249-56
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • Obesity is a worldwide epidemic, threatening both industrialized and developing countries, and is accompanied by a dramatic increase in obesity-related disorders, including type 2 diabetes mellitus, hypertension, cardiovascular diseases, and nonalcoholic fatty liver disease. Recent studies have shown that the gut microbial community (microbiota) is an environmental factor that regulates obesity by increasing energy harvest from the diet and by regulating peripheral metabolism. However, there are no data on how obesogenic microbiotas are established and whether this process is determined during infancy. The sterile fetus is born into a microbial world and is immediately colonized by numerous species originating from the surrounding ecosystems, especially the maternal vaginal and fecal microflora. This initial microbiota develops into a complex ecosystem in a predictable fashion determined by internal (eg, oxygen depletion) and external (eg, mode of birth, impact of environment, diet, hospitalization, application of antibiotics) factors. We discuss how the gut microbiota regulates obesity and how environmental factors that affect the establishment of the gut microbiota during infancy may contribute to obesity later in life.
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10.
  • Schéle, Erik, 1980, et al. (creator_code:aut_t)
  • Regulation of body fat mass by the gut microbiota: Possible mediation by the brain.
  • 2016
  • record:In_t: Peptides. - : Elsevier BV. - 1873-5169 .- 0196-9781. ; 77
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • New insight suggests gut microbiota as a component in energy balance. However, the underlying mechanisms by which gut microbiota can impact metabolic regulation is unclear. A recent study from our lab shows, for the first time, a link between gut microbiota and energy balance circuitries in the hypothalamus and brainstem. In this article we will review this study further.
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