Effects of dietary fat profile on gut permeability and microbiota and their relationships with metabolic changes in mice

Lam, Yan Y.; Ha, Connie; Hoffmann, Jenny; Oscarsson, Jan; Dinudom, Anuwat; Mather, Thomas J.; Cook, David I.; Hunt, Nicholas H.; Caterson, Ian D.; Holmes, Andrew; Storlien, L. H.

doi:10.1002/oby.21122

Cited by 173 publications

(145 citation statements)

References 41 publications

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“…In mice, a high-fat saturated fat diet, but not a high omega-6 fatty acid diet, increased colonic permeability and mesenteric fat inflammation (128). The high saturated-fat diet was associated with decreased hydrogen-sulfide producing bacteria, and a large portion of the variability in intestinal variability could be accounted for by hydrogen-sulfide producing bacteria (128). Fish oil reduced the inflammation elicited by the high saturated fat diet (128).…”

Section: Diet Modulates Absorption Of Bacterial Componentsmentioning

confidence: 99%

“…The high saturated-fat diet was associated with decreased hydrogen-sulfide producing bacteria, and a large portion of the variability in intestinal variability could be accounted for by hydrogen-sulfide producing bacteria (128). Fish oil reduced the inflammation elicited by the high saturated fat diet (128). Fish oils have also been shown to counteract the dysbiotic effects of high omega-6 fatty acid diets under normal conditions, but in the case of frank sepsis fish oils impair the detoxification of LPS (129).…”

Section: Diet Modulates Absorption Of Bacterial Componentsmentioning

confidence: 99%

“…For example, bacteria trans-located into mesenteric fat as determined by presence of the 16S bacterial gene, and this correlated positively with changes in intestinal permeability (128). In order to identify factors that affect systemic exposures to intestinal bacteria in clinical trials, biomarkers of exposures are needed.…”

Section: Biomarkers Of Systemic Bacterial Exposuresmentioning

confidence: 99%

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Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Djurić

2017

Translational Research

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Obesity increases the risks of many cancers. One important mechanism behind this association is the obesity-associated pro-inflammatory state. Although the composition of the intestinal microbiome undoubtedly can contribute to the pro-inflammatory state, perhaps the most important aspect of host-microbiome interactions is host exposure to components of intestinal bacteria that stimulate the inflammatory reactions. Systemic exposures to intestinal bacteria can be modulated by dietary factors by altering both the composition of the intestinal microbiota as well as absorption of bacterial products from the intestinal lumen. In particular, high fat and high energy diets have been shown to facilitate absorption of bacterial lipopolysaccharide (LPS) from intestinal bacteria. Biomarkers of bacterial exposures that have been measured in blood include LPS-binding protein, sCD14, fatty acids characteristic of intestinal bacteria and immunoglobulins specific for bacterial LPS and flagellin. The optimal strategies to reduce these pro-inflammatory exposures, whether by altering diet composition, avoiding a positive energy balance or reducing adipose stores, likely differ in each individual. Biomarkers that assess systemic bacterial exposures therefore should be useful to optimize and personalize preventive approaches for individuals and groups with specific characteristics, and to gain insight into the possible mechanisms involved with different preventive approaches.

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Section: Diet Modulates Absorption Of Bacterial Componentsmentioning

confidence: 99%

Section: Diet Modulates Absorption Of Bacterial Componentsmentioning

confidence: 99%

Section: Biomarkers Of Systemic Bacterial Exposuresmentioning

confidence: 99%

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Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Djurić

2017

Translational Research

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“…However these responses are transient; it is long-term processes that primarily contribute to chronic community state development. For example, in mice fed a high-fat diet, it typically takes >6 weeks for a community state characteristic of diet-induced obesity to appear (16, 17). Here the appearance of “inflammophilic pathobionts” follows development of an inflammatory state and increased intestinal permeability (17).…”

Section: Introductionmentioning

confidence: 99%

Towards an Integrative Understanding of Diet–Host–Gut Microbiome Interactions

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Holmes

2017

Front. Immunol.

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Over the last 20 years, a sizeable body of research has linked the microbiome and host diet to a remarkable diversity of diseases. Yet, unifying principles of microbiome assembly or function, at levels required to rationally manipulate a specific individual’s microbiome to their benefit, have not emerged. A key driver of both community composition and activity is the host diet, but diet–microbiome interactions cannot be characterized without consideration of host–diet interactions such as appetite and digestion. This becomes even more complex if health outcomes are to be explored, as microbes engage in multiple interactions and feedback pathways with the host. Here, we review these interactions and set forth the need to build conceptual models of the diet–microbiome–host axes that draw out the key principles governing this system’s dynamics. We highlight how “units of response,” characterizations of similarly behaving microbes, do not correlate consistently with microbial sequence relatedness, raising a challenge for relating high-throughput data sets to conceptual models. Furthermore, they are question-specific; responses to resource environment may be captured at higher taxonomic levels, but capturing microbial products that depend on networks of different interacting populations, such as short-chain fatty acid production through anaerobic fermentation, can require consideration of the entire community. We posit that integrative approaches to teasing apart diet–microbe–host interactions will help bridge between experimental data sets and conceptual models and will be of value in formulating predictive models.

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“…Tanto em modelos animais, quanto em humanos, alimentação rica em gorduras é capaz de induzir alterações na microbiota e isso foi correlacionado com a gravidade da síndrome metabólica, que possui uma forte influência do sistema imune (66).…”

Section: Receptores Da Imunidade Inata No Desenvolvimento Da Obesidadunclassified

MyD88: um modulador do perfil inflamatório e metabólico na obesidade experimental.

Castoldi¹

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RESUMOIntrodução: Nos últimos anos, a ativação de receptores da imunidade inata nas células do sistema imune e no tecido adiposo foi descrita como crucial durante o desenvolvimento da obesidade. Além disso, alterações na microbiota intestinal foram relacionadas aos fenótipos inflamatórios e metabólicos na obesidade através do aumento da permeabilidade intestinal, com elevação dos níveis sistêmicos de endotoxina, que colabora para o aumento da inflamação e o desenvolvimento da resistência à insulina. A complexidade do sistema imune nos permite explorar essas vias de sinalização nos diversos órgãos, tecidos e células. Por isso formulamos a hipótese de que MyD88 regularia o desenvolvimento da obesidade, desempenhando um papel importante no tecido adiposo contribuindo para a resistência à insulina. Nos macrófagos, a sinalização via MyD88 favoreceria um perfil pró-inflamatório, e ainda, regularia alterações na microbiota intestinal que por sua vez estariam contribuindo nesse processo através de alterações na permeabilidade intestinal. Objetivo: Estudar a relação entre a obesidade e inflamação, focando no papel da molécula adaptadora MyD88 e sua importância no tecido adiposo, macrófagos, intestino e na modulação da microbiota intestinal. Métodos: Utilizamos camundongos C57BL/6, deficientes de MyD88 (KO), Adiponectina cre+ MyD88 flox +/+ e Lisozima cre+ MyD88 flox +/+ alimentados com dieta hiperlipídica e avaliamos os perfis metabólicos e inflamatórios, permeabilidade intestinal e alterações na microbiota intestinal. Ainda em um modelo de transplante de microbiota estudamos o possível papel da microbiota no desenvolvimento da obesidade. Resultados: Verificamos que camundongos MyD88 KO ganharam mais peso comparados aos camundongos WT, são mais intolerantes à glicose e resistentes à insulina. Porém, ao analisarmos o perfil inflamatório no tecido adiposo e sistêmico, observamos significativa diminuição de IL-1β, TNF-α e IL-6 bem como diminuição na fosforilação das vias de sinalização pró-inflamatórias nos camundongos MyD88 KO obesos. No tecido adiposo, há um predomínio de macrófagos de perfil M1. Além disso, observamos menor inflamação no intestino, porém, a permeabilidade intestinal estava aumentada. A microbiota dos camundongos MyD88 KO foi capaz de induzir resistência à insulina nos camundongos WT, aumentou a permeabilidade intestinal e inflamação no tecido adiposo. A depleção de MyD88 no tecido adiposo não alterou o perfil metabólico dos camundongos comparados aos controles. No entanto, a depleção de MyD88 nos macrófagos, protegeu os camundongos do ganho de peso, resistência à insulina e do aumento da permeabilidade intestinal. Observamos maior polarização M2 no tecido adiposo desses camundongos. Ainda, camundongos MyD88 KO obesos não foram capazes de montar uma resposta inflamatória em resposta à sepse. No entanto, no tecido adiposo dos camundongos MyD88 KO obesos, observamos um aumento significativo da expressão de Dectina-1 e IFN-β, o que poderia explicar a resistência à insulina com a ausência da inflamação clássi...

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Effects of dietary fat profile on gut permeability and microbiota and their relationships with metabolic changes in mice

Cited by 173 publications

References 41 publications

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Towards an Integrative Understanding of Diet–Host–Gut Microbiome Interactions

MyD88: um modulador do perfil inflamatório e metabólico na obesidade experimental.

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