Tlr4 At The Crossroads Of Nutrients, Gut Microbiota, And Metabolic Inflammation

dc.creatorVelloso
dc.creatorLicio A.; Folli
dc.creatorFranco; Saad
dc.creatorMario J.
dc.date2015-JUN
dc.date2016-06-07T13:16:31Z
dc.date2016-06-07T13:16:31Z
dc.date.accessioned2018-03-29T01:37:07Z
dc.date.available2018-03-29T01:37:07Z
dc.identifier
dc.identifierTlr4 At The Crossroads Of Nutrients, Gut Microbiota, And Metabolic Inflammation. Endocrine Soc, v. 36, p. 245-271 JUN-2015.
dc.identifier0163-769X
dc.identifierWOS:000357726000001
dc.identifier10.1210/er.2014-1100
dc.identifierhttp://press.endocrine.org/doi/10.1210/er.2014-1100?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/242106
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1305804
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionObesity is accompanied by the activation of low-grade inflammatory activity in metabolically relevant tissues. Studies have shown that obesity-associated insulin resistance results from the inflammatory targeting and inhibition of key proteins of the insulin-signaling pathway. At least three apparently distinct mechanisms-endoplasmic reticulum stress, toll-like receptor (TLR) 4 activation, and changes in gut microbiota-have been identified as triggers of obesity associated metabolic inflammation; thus, they are expected to represent potential targets for the treatment of obesity and its comorbidities. Here, we review the data that place TLR4 in the center of the events that connect the consumption of dietary fats with metabolic inflammation and insulin resistance. Changes in the gut microbiota can lead to reduced integrity of the intestinal barrier, leading to increased leakage of lipopolysaccharides and fatty acids, which can act upon TLR4 to activate systemic inflammation. Fatty acids can also trigger endoplasmic reticulum stress, which can be further stimulated by cross talk with active TLR4. Thus, the current data support a connection among the three main triggers of metabolic inflammation, and TLR4 emerges as a link among all of these mechanisms.
dc.description36
dc.description3
dc.description
dc.description245
dc.description271
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description
dc.description
dc.description
dc.languageen
dc.publisherENDOCRINE SOC
dc.publisher
dc.publisherWASHINGTON
dc.relationENDOCRINE REVIEWS
dc.rightsfechado
dc.sourceWOS
dc.subjectEndoplasmic-reticulum Stress
dc.subjectInsulin-receptor Substrate-1
dc.subjectDiet-induced Obesity
dc.subjectNf-kappa-b
dc.subjectToll-like Receptor-4
dc.subjectFree Fatty-acids
dc.subjectNecrosis-factor-alpha
dc.subjectPhosphatidylinositol 3-kinase Activity
dc.subjectType-2 Diabetes-mellitus
dc.subjectBeta-cell Apoptosis
dc.titleTlr4 At The Crossroads Of Nutrients, Gut Microbiota, And Metabolic Inflammation
dc.typeArtículos de revistas
dc.typeResumo


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