ArticleSurgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery2021
Toll-like receptor 4 and myeloid differentiation factor 88 are required for gastric bypass-induced metabolic effects.
Article in Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Oral microbiota-driven immune modulation along the oral-gut axis: from local signals to systemic inflammation.NPJ biofilms and microbiomes · 2026Review
- Toll-like Receptor 4 Differentially Modulates Cardiac Function in Response to Chronic Exposure to High-Fat Diet and Pressure Overload.Nutrients · 2023Article
- Might Gut Microbiota Be a Target for a Personalized Therapeutic Approach in Patients Affected by Atherosclerosis Disease?Journal of personalized medicine · 2023Review
- Regulation of body weight: Lessons learned from bariatric surgery.Molecular metabolism · 2023Review
- Bariatric surgery for diabetic comorbidities: A focus on hepatic, cardiac and renal fibrosis.Frontiers in pharmacology · 2022Review
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10 authors.
Funding
Abstract
backgroundToll-like receptor 4 (TLR4) has been suggested as one of the forefront cross-communicators between the intestinal bacteria and the host to regulate inflammatory signals and energy homeostasis. High-fat diet-induced inflammation is mediated by changes in gut microbiota and requires a functional TLR-4, the deficiency of which renders mice resistant to diet-induced obesity and its associated metabolic dysfunction. Furthermore, gut microbiota was suggested to play a key role in the beneficial effects of Roux-en-Y gastric bypass (RYGB), a commonly performed bariatric procedure.
objectivesTo explore whether TLR4, myeloid differentiation factor 8 (MyD88; 1 of its key downstream signaling regulators) and gut microbiota play an integrative role in RYGB-induced metabolic outcomes.
settingAnimal- based study.
methodWe performed RYGB in TLR4 and MyD88 knock-out (KO) mice and used fecal microbiota transplant (FMT) from RYGB-operated animals to these genetic mouse models to address our questions.
resultsWe demonstrate that RYGB reduces TLR4 expression explicitly in the small and large intestine of C57Blc/6J mice. We also show that TLR4 KO mice have an attenuated glucoregulatory response to RYGB. In addition, we reveal that MyD88 KO mice fail to respond to all RYGB-induced metabolic effects. Finally, fecal microbiota transplant from RYGB-operated mice into TLR4 KO and MyD88 KO naïve recipients fails to induce a metabolic phenotype similar to that of the donors, as it does in wild-type recipients.
conclusionTLR4 and MyD88 are required for RYGB-induced metabolic response that is likely mediated by gut microbiome.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.