Digital public defece: Ayodeji Awoyemi
MD Ayodeji Awoyemi at Institute of Clinical Medicine will be defending the thesis Microbial translocation and cardiovascular disease states. Emphasis on chronic heart failure, diabetes and the metabolic syndrome for the degree of PhD (Philosophiae Doctor).
Photo: ESC Congress 2018,
Speaker Service Centre Photo Booth
The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital trial lecture - time and place
- First opponent: Professor Thomas Lüscher, Imperial College London, United Kingdom
- Second opponent: Professor Jan Kristian Damås, Norwegian University of Science and Technology, Trondheim
- Third member and chair of the evaluation committee: Associate Professor Kristina Haugaa, Institute of Clinical Medicine, University of Oslo
Chair of defence
Professor II Dan Atar, Institute of Clinical Medicine, University of Oslo
Ingebjørg Seljeflot, Institute of Clinical Medicine, University of Oslo
The gut microbiota has recently emerged as a potential treatment target in cardiovascular disease (CVD). Leakage of bacterial wall products and the production of microbial diet-dependent metabolites such as trimethylamine-N-oxide (TMAO), have been hypothesized to contribute to both initiation and progression of CVD.
We hypothesized that gut leakage through systemic inflammation is associated with metabolic syndrome and CVD and that modulation of the gut microbiota with diet intervention or omega-3 fatty acids, can reduce gut leakage and subsequently inflammation. Furthermore, that modulation of the gut microbiota with probiotics or antibiotics can improve cardiac function in chronic heart failure and reduce markers of gut leakage, systemic inflammation and TMAO.
We found that high levels of gut leakage markers were associated with an increased risk of having metabolic syndrome in a high CVD risk population. Furthermore, high levels of the gut leakage marker lipopolysaccharide binding protein (LBP) was associated with a 2-fold increased risk of developing CVD in the 3-year follow-up period. Neither omega-3 fatty acid supplementation nor diet intervention had any effect on the markers in this population.
In heart failure, neither the locally acting antibiotic rifaximin nor the probiotic yeast Saccharomyces boulardii had any effect on cardiac function after 3 months’ treatment. Furthermore, both intervention did not significantly affect any marker of gut leakage, systemic inflammation, the metabolite TMAO and importantly the gut microbiota diversity. High levels of gut leakage markers did however predict high levels of N-terminal pro-Brain Natriuretic Peptide (NT-ProBNP), a surrogate marker of cardiac function.
Our studies suggests that the gut microbiota may play a role in CVD. Before we can conclude with a causal role in CVD, we need to sort out modalities that safely and effectively can change the microbiota and reduce the leakage markers.
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